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This time we're going to look at a beautiful portrait of what the Lord Jesus Christ has done for us. And we're going to find it in a most unusual place. The story opens in the backside of nowhere—a place called Lo-debar. This month of December, let's look at and study a very different Christmas story. Let's turn our minds to a time long ago, to what could have been private thoughts and fears inspired by the account in the book of 2 Samuel.
She stood in the doorway, gazing idly across the barren landscape of Lo-debar. The day stretched ahead as empty as yesterday…and the day before that, and the weeks—even years—before that.
Lo-debar was "nowhere."
"How aptly named," she thought, for Lo-debar meant place of no pasture. But it provided safety. And it was a good hiding place. That made it perfect.
She had done her duty to her young charge. Faithfully she cared for Mephibosheth, Jonathan's son, the only surviving heir of King Saul. She'd come to love him as her own. His safety was all that mattered.
Years ago she had fled in stark terror, fearing for his life, when it appeared David's army might seek him out and kill him. In haste she snatched him up, and running… tripping… falling upon the child… she crippled him for life.
Yes, David was Jehovah's anointed to take over the throne of Israel. Grudgingly, she admitted that. But was this—this barren, useless life—the life Jehovah ordained for Mephibosheth? Son of Jonathan, David's dearest friend and covenant brother?
Daily she dreamed about what their lives might have been. If only Jonathan had lived to see David take the throne! He'd have been David's trusted advisor as well as closest friend. And Mephibosheth's life? Oh, so different! As Jonathan's son, he'd be coming and going freely from the palace that had once been his grandfather's, training as a soldier alongside his valiant father who had defied King Saul himself to keep his covenant with David.
But Saul declared himself David's bitterest enemy, and when he died in battle, Jonathan died alongside him, and with them both, Mephibosheth's future. David's followers might leave no heir of Saul's alive.
Mephibosheth pulled himself to her side in the doorway. Together they looked out on another day in this dusty hideaway. He had been heir to the throne. Now he served a life-sentence in solitude.
Something stirred in the distance. A cloud? Maybe another dust-devil scudding across the horizon. But this one grew in size. And it was coming their way.
This was no dust cloud. Armed men approached on horseback—they weren't passing a safe distance away. Fear gripped her again. They were headed straight for Lo-debar, and this time there was no place to flee. Life as they knew it was about to end.
What, you ask, does this bleak picture of the later life of Jonathan's son have to do with Christmas? With the promised coming of the Messiah? With Immanuel—"God with us"? So much!—as we are about to find out. Though Mephibosheth's loving caregiver could not know at that moment—and neither did he—Christmas had just come to Lo-debar. And it came through the work of…the Blood Covenant.
In an instant, Mephibosheth was about to be transferred from loneliness, poverty, isolation from his family and heritage, and placed right into that family seated at King David's table, adopted by the king, coming under his protection forever, welcomed as a beloved—all because of the promise the king had made and was going to honor.
Christmas and the Blood Covenant are locked together. The Lord Jesus Christ was sent by God ("the Word became flesh") to fulfill the Father's promise, and through His blood all of Abraham's descendants and all the sons and daughters of Adam can be forgiven, redeemed, and accepted by the Father.
In the life of the wounded, limping, abandoned and forgotten Mephibosheth, there is a beautiful portrait of what Christmas truly means to us. For, dear friend, you and I are Mephibosheth.
Have you ever thought of Philippians 2:6-7 as a Christmas passage? Well, it is! Paul paints for us in these verses the most glorious picture of what it really meant for the Second Person of the Trinity to commit Himself fully to the Blood Covenant.
1. Turn to Philippians 2:6.
6 Who, being in the _______ ____ God, thought it not robbery to be _________ with God:
This translation makes it difficult to know what Paul is saying here. The Amplified Bible makes it clear:
6 "…although being essentially one with God and in the form of God [possessing the fullness of the attributes which make God God], did not think this equality with God was a thing to be eagerly grasped or retained…."
(Philippians 2:6, Amplified Bible)
2. Continue to verse 7:
7 But made Himself of ___ ________________, and took upon Him the form of a ________________ , and was made in the ________________ of _______:
Better explained:
7 …stripped Himself of all privileges and rightful dignity, so as to assume the guise of a servant, in that He became like men and was born a human being." (Philippians 2:7, Amplified Bible)
Mary, His mother, and Bethlehem's manger were the first to cradle the King who stepped out of Heaven's glory to become our sacrifice for sin.
Philippians isn't the only unexpected place where you'll find The Christmas Story.
3. Turn in your Bible to the book of First Samuel. First Samuel as a Christmas study? Yes. Let's begin with chapters 17, 18, and 19.
What event, one of the most famous accounts in Old Testament history, has just occurred in 1 Samuel 17?
4. The last verse (v. 58) of this chapter has Saul asking David a question. What was David's simple answer?
What character trait does this reveal about David?
5. The very next verse of Scripture (18:1) shows the beginning of the friendship between David and Jonathan. Fill in this verse for a picture of how Jonathan felt about David.
1And it came to pass, when he [David] had made an end of speaking unto Saul, that the _________ of Jonathan was knit with the ________ of David, and Jonathan _________ him as his own ________.
Sometimes in life we meet someone with whom we have an instant connection—we feel as though we've known them all our lives. This was how it was with David and Jonathan.
2 Saul took him that day, and would not let him go home to his father's house.
King Saul said, "David, I want you to be my son also. You come to my house."
6. 1 Samuel 18:3 is one of the key verses of our study:
3Then Jonathan and David _______ a _______________, because he loved him as his own soul.
What is a "Blood Covenant? Blood covenants go all the way back to the book of Genesis. The word "covenant" comes from a root word that means "to cut." In fact, the Old Testament phrase is literally "to cut a covenant." When a living being—person or animal—is cut, blood flows. To make a covenant literally involves blood. Many of us have seen in old movie westerns two people making a blood covenant. They get together, decide there should be peace, each makes an incision on his wrist, then they join their hands together, let the blood mingle and lift them to heaven in a promise, a covenant. "There will be no more war. We are now blood brothers." It was a co-mingling of lives. "The life of the flesh is in the blood" (Lev. 17:11).The scar that remained would be called "the mark of the covenant." Those who were in covenant were called "friends.
What is a "Blood Covenant? Blood covenants go all the way back to the book of Genesis. The word "covenant" comes from a root word that means "to cut." In fact, the Old Testament phrase is literally "to cut a covenant." When a living being—person or animal—is cut, blood flows. To make a covenant literally involves blood. Many of us have seen in old movie westerns two people making a blood covenant. They get together, decide there should be peace, each makes an incision on his wrist, then they join their hands together, let the blood mingle and lift them to heaven in a promise, a covenant. "There will be no more war. We are now blood brothers." It was a co-mingling of lives. "The life of the flesh is in the blood" (Lev. 17:11).The scar that remained would be called "the mark of the covenant." Those who were in covenant were called "friends.
The whole Bible is about a blood covenant.
You know that the Bible is divided into two halves, Old Testament and New Testament, and that the words "testament" and "covenant" are the same word. We could just as easily say the Bible is divided into the Old Covenant and the New Covenant. All the promises in the Bible are covenant promises.
7. Turn to Psalm 25:14. "The secret of the Lord is with them that fear Him, and He will show them His ___________________."
8. Turn to Luke 22:20. When the Lord Jesus Christ met with His disciples for The Last Supper, He said,
"This cup is the new __________________ in My blood, which is shed for you."
When we come to the Lord's Table, we are celebrating the blood covenant.
8. Turn back to 1 Samuel 18:4. As part of their covenant, Jonathan gave David some symbolic items.
4And Jonathan stripped himself of the _________ that was upon him, and gave it to David, and his _____________, even to his ____________, and to his _______, and to his girdle [belt].
a. A Robe
This symbol marked Jonathan out as the king's son. It spoke of his position. He's saying, "I'm yielding my position over to you. I want David in my place." That ought to be true of every follower of the Lord Jesus Christ, with whom we are in blood covenant. "Lord, I yield my position in life over to You."
b. Garments
The clothing spoke of his possessions. He's saying, "David, all I have belongs to you, because if it were not for you, I really wouldn't have anything. You won the victory for me."
c. Sword and Bow
Two weapons of warfare. These spoke of Jonathan's power. In essence he's saying, "You deserve everything. You have won my loyalty; I'm committed to you; all I have is yours. I know how to use this bow, but I have no longer any right to self-defense. I yield that over to you. And David, your battles are my battles. My weapons of war now belong to you. My position is yours! My possessions are yours! My power is yours! I give it over to you! We are now blood brothers!"
That's what "covenant" meant. Covenant and commitment go hand-in-hand.
Covenant Keepers Show "Lovingkindness"
People in covenant one with another show "lovingkindness" to each other. It's going to come into play for Mephibosheth. But what precisely is "lovingkindness"?
"Lovingkindness" [Hebrew: hesed] is a word seen throughout the Old Testament. In the Book of Psalms alone, it is found 24 times! Some have said it is the Old Testament version of the New Testament word for God's love [Greek: agape]. It is complete and total, the highest form of love, the love God showered upon us because of His character and Who He is, out of His great love, not upon our works or merit. Example: "For God so loved [agaped] the world that He gave His only begotten Son."
Lovingkindness means "I will do you good, regardless, because we are in covenant together. You can call upon me as your friend, and I will show you lovingkindness, because we are now blood brothers. We have made a covenant."
"Lovingkindness" [Hebrew: hesed] is a word seen throughout the Old Testament. In the Book of Psalms alone, it is found 24 times! Some have said it is the Old Testament version of the New Testament word for God's love [Greek: agape]. It is complete and total, the highest form of love, the love God showered upon us because of His character and Who He is, out of His great love, not upon our works or merit. Example: "For God so loved [agaped] the world that He gave His only begotten Son."
Lovingkindness means "I will do you good, regardless, because we are in covenant together. You can call upon me as your friend, and I will show you lovingkindness, because we are now blood brothers. We have made a covenant."
This was the love David and Jonathan had for each other. Their covenant was not only between the two of them but applied to their offspring. The children of those in covenant are a part of the covenant. If they will ratify the covenant, they, too, will receive its benefits. "Lovingkindness" and the Blood Covenant transformed Mephibosheth's story—and ours.
Let's go back in time to just before the day that "Christmas" came to Lo-debar. When David began receiving praise from the people, King Saul, insane with jealousy, sent out a royal edict that David must be killed. Jonathan was in a closer relationship to David than to his own natural father (just as we in Christ are sometimes closer to our brothers and sisters in Christ than to members of our natural family).
Saul began to hunt David like a wild partridge on the hills of Judea. All the forces of the kingdom were focused: find David, kill David; find David, kill David.
David fled for his life. But Saul and Jonathan were both slain in battle. David, God's anointed, was now king. There was blind panic in the kingdom among Saul and Jonathan's families.
Can you imagine the emotions running through the land when David is suddenly the king? Until this point, everyone has been saying, "Find David, kill David." Now David is king! They're wondering, "When will the retaliation begin? When will David take vengeance on his enemies?"
And so little Mephibosheth came to be crippled, hidden, exiled. All his nurse knows is that there is another king who is going to come and take vengeance.
How many times the child must have asked,
"Why am I here?"
"You're here because someone's trying to kill you."
"Why am I crippled?"
"Because we were running from him."
"What's going to happen?"
"You better hope he never finds you."
Mephibosheth grew up with this lesson embedded: fear David, hate David; fear David, hate David. There he is, dragging his crippled limbs, eating dust, breathing dust, drinking from a tin cup, a prince in exile.
Remember we said earlier, "You and I are Mephibosheth." Dear friend, before the manger in Bethlehem cradled a king, you and I were Mephibosheth—exiled from our King, crippled, drinking from a tin cup. In the Garden, before the Fall, we had been destined to inherit everything, to rule and reign. Then we lost the destiny God originally had for us.
9. Turn now to 2 Samuel 9:1. Prepare to be blessed! Peace has once again been restored. The infighting is over. David, with a little down-time on his hands, remembers his covenant with Jonathan.
"And David said, Is there _____ yet that is _______ of the house of ________ that I may show him kindness for _____________________ sake? And there was of the house of Saul a servant, whose name was Ziba. And when they had called him unto David, the king said unto him, Art thou Ziba? And he said, Thy servant is he. And the king said, __________________________________________________________________?"
About this time people in the court were probably thinking, "Hah! Here it comes; we wondered when the purge would begin."
But David, now the king, wants to fulfill the covenant he made with Jonathan and show kindness to Mephibosheth. He'd never met him before, but he is in covenant with Mephibosheth's father, Jonathan.
David says, "Go fetch him. Bring him to me."
Out from the palace thundered royal troops, the king's men. Out to Lo-debar.
Can you see Mephibosheth as the dust cloud brings the horses right to his door?
"Oh no! He's found me!"
They push open the door. "Are you Mephibosheth?"
"Come with us."
"The king wants you."
Mephibosheth lowers his eyes to the ground. He looks one last time at the dirt floor under his crippled feet. As the horse beneath him jostles him away, he looks back to the only home he can remember. Desolate though it was, at least he had been safe there.
As they bring him before King David, we might wonder, did he have any memory of the palace as it had been? Was he thinking of the life he lost? Casting his crutches aside, he falls on his face before the king and begins to tremble like a bird in a trap.
10. Turn to 2 Samuel 9:7 and 8—
"And David said unto him, Fear not; for I will surely show thee _____________ for ________________ thy father's sake, and I will ____________ unto thee all the land of Saul, thy father; and thou shalt eat bread at my table continually."
To this one who is expecting death, King David says, "I want to restore your inheritance. I want you to dine at my table. I want you to be like my son."
Mephibosheth can hardly take it in.
"And he ____________ himself, and said, What is thy servant, that thou shouldest look upon such a _______ ______ as I?" (v. 8)
["I'm as good as dead. Why would you want to give me back my inheritance? Why would you want me to eat at your table? Why would you want me to be as your son?"]
Is Mephibosheth not exactly as we once were, before we knew Christ, and before the Cross? But now we are Beloved in Christ.
11. Turn to 1 Corinthians 6:9-11. Paul is writing to the family of God in Corinth.
9 Know ye not that the __________________shall not _____________ the _______________of God? Be not deceived: neither fornicators, nor idolaters, nor adulterers, nor effeminate, nor abusers of themselves with mankind,
10 Nor thieves, nor covetous, nor drunkards, nor revilers, nor extortioners, shall inherit the kingdom of God.
11 And such were some of you: but ye are _____________, but ye are _________________, but ye are __________________ in the name of the Lord Jesus, and by the Spirit of our God.
We, like Mephibosheth, are inheriting what we do not deserve through the Blood Covenant.
There were animal sacrifices to cover and atone for the people's sins. But before the Cross, there had never been that full restoration where we could call God our "Father."
12. Turn to Matthew 6:9. When Jesus came to earth and taught His disciples to pray, what were the first two words of what we now call "The Lord's Prayer"?
In this manner, therefore, pray: _______ ____________ in heaven, Hallowed be Your name.
Before Jesus, no one ventured to address God as "Father." When Jesus came, He changed all that. He continually said, "Father."
Imagine David saying, "Now Mephibosheth, I want you to understand, it's not a matter of any accomplishment on your part. It's my love for Jonathan. And for his sake, I'm keeping our blood covenant."
To this point Mephibosheth had seen David the king as an enemy and a threat. And he's been hiding from him. At this moment he has a decision to make. If he wants to, he can ratify the covenant. No longer is David an enemy; now David is a friend. No longer is he out of fellowship with David; he's in fellowship with David. No longer is he running from David, he is running to David. He must
Does that sound familiar to you? Those are the terms of salvation in the New Testament: repentance and faith!
Of course, Mephibosheth ratified the covenant! Once he does, transformation takes place. Christmas came to the lowly resident of Lo-debar. He's transferred to the palace of the king!
Christmas Restores the Promised Inheritance
13. Turn now to 2 Samuel 9:9.
"Then the king called Ziba, Saul's servant, and said unto him, I have given unto thy _______________'s _______ [Mephibosheth] all that pertaineth to Saul and to all his house," [I'm giving him all of the wealth that his grandfather had]. "Thou, therefore, and thy sons, and thy servants, shall _____ ____ ______ ____ ______," [just take care of all of this land that belongs to him now] "and thou shalt bring in the fruits, that thy master's son may have food to eat; ______ Mephibosheth, thy master's son, shall eat bread __________ at ____ ___________."
Imagine the transformation Yesterday Mephibosheth is living in Lo-debar, on the backside of nowhere, crippled, eating and breathing dust, and this morning he awakens on silken sheets in the palace. Servants arrive to meet his every need, saying, "The king and his sons are waiting for you. You're coming to breakfast in the palace."
14. How many times in chapter 9 does David say Mephibosheth will "eat at my table"?
He comes down to breakfast and there's the king at a table groaning with food. There's a white linen tablecloth. His misshapen limbs are under the tablecloth and can't even be seen.
Is this not a picture of what Jesus does for us? He covers us with His righteousness. He clothes us in pure white linen.
15. Turn to Revelation 7:9.
After this I beheld, and, lo, a great multitude, which no man could number, of all nations, and kindreds, and people, and tongues, stood before the throne, and before the Lamb, clothed with __________ ___________…"
Mephibosheth is thinking, "I can't understand this. I don't deserve this. Yet it's because of a blood covenant. It is a covenant my father made with David. I can't completely understand it, but I can't deny it. Here I am! Pass the biscuits!"
And as David passes the bread, there's a scar on David's wrist. The mark of the covenant the king once made. It dawns on Mephibosheth: the power of a blood covenant.
Each time we come to the Lord's Supper, Jesus is passing the bread to us. One day, we will be brought to the Marriage Supper of the Lamb. Jesus will break bread and pass it to us.
16. Turn to Luke 22:19-21. The next time you partake of the Lord's Supper, you will have even greater appreciation for what Jesus said:
19And he took bread, and gave thanks, and brake it, and gave unto them, saying, "This is My body which is given for you: this do in remembrance of Me." 20Likewise also the cup after supper, saying, "This cup is the new ___________________ in My ___________, which is shed for you…"
How wonderful to understand this Christmas season the saving power of the blood covenant. God was made flesh that there might be a blood covenant with you. 2000 years ago, Jesus entered into a blood covenant with God the Father for the sons and daughters of Adam.
Many people, like Mephibosheth, find themselves running from and fearing God. God is love. God loves you. And God has made with His Son, the Lord Jesus, a blood covenant on your behalf.
13. Turn back to 2 Samuel 9:1 and keep that place while turning to Ephesians 4:32. Note the comparison.
2 Samuel 9:1— "And David said, Is there any yet that is left of the house of Saul that I may show him kindness _____ ________________'s __________?"
Ephesians 4:23—"Be ye kind, tenderhearted, forgiving one another, even as God _______ ______________'s _________ hath forgiven you."
Mephibosheth hated/feared David Lost man fears/hates God
Mephibosheth was not worthy We are not worthy
Mephibosheth was deformed by a fall We are deformed by the Fall
Mephibosheth was "a dead dog" We were under the sentence of death
God gave Adam the earth to rule and reign. Through sin Adam lost it. But God made a covenant. There would be a Redeemer. Jesus has restored it! We're heirs of God and joint-heirs with the Lord Jesus Christ. And God, for Christ's sake, has forgiven us.
Because of the Blood Covenant:
Mephibosheth now has: We now have:
the king's forgiveness the King's forgiveness
a fortune restored a fortune restored
fellowship with the king fellowship with the King
Sometimes the devil will whisper to you: "You're not worthy."
Don't argue with him. You'll lose the argument. You're not worthy.
Point him to the Blood Covenant and back out of the argument.
Let him take up his argument with Almighty God and the Blood Covenant.
There was a time, centuries before Bethlehem, when Christmas came to Lo-debar. When a cripple received the benefit of the covenant made by his father and was ushered into the king's presence.
When you celebrate Christmas this year, when you see the child in the manger, when you see the lights, hear the carols, the music, the laughter,
Our God is a faithful, covenant-keeping God. We have moved from exile, loneliness and desolation into relationship with him. Mephibosheth must have been dazzled by all he now had access to.
Are you truly aware of all you now have access to?
The Creator of the universe as your own Heavenly Father.
Access to His throne of grace any time.
The privilege of speaking with Him, day or night.
And if you ask for it, His guidance directing your life.
Through his story, this Christmas you will understand where you stand with God because…
Long ago your Heavenly Father made a blood covenant.
Your elder brother, the Lord Jesus Christ, sealed it with His blood.
And you are brought into the palace of the King, to live in relationship with Him. Starting now, and for eternity.
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text: In the days of Black Sails, pirates knew no boundaries, and they acknowledged no government rule. They flew the flag of their ship – and the sight of a pirate flag often spelled mayhem and doom for any crew who encountered it. VIP Fan Auctions is offering one of the most memorable pirate flags from Black Sails – the red skeleton holding a bleeding heart, which flew on the ship of Captain Ned Low, an ill-tempered pirate captain notorious for brutality, in the second-season premiere of the Starz epic. The flag is impressive (pictured above flying off the stern of the ship), measuring 12×19 feet and a bit tattered from battle and the elements. Click here for photos and more information, and claim your own pirate flag straight from the seas of Black Sails!

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text: I was hearing about this recent court ruling in AU this week and would love to hear a few different takes on it. Now first, because the ruling was a juvenile the public records are spotty. But from what I can tell the Courts in AU have forced the parents of a ten year old to begin medical treatments to suspend puberty in 10 year old boy who self identifies as a girl. First, I have no problem with adults getting a sex change operation. It's basically their own and no one else's business. And obviously there are rare cases that happen when the physical sex of a child is not clear at birth due to some abnormality. But when I hear of eight year olds insisting that they are sexually mis-identified I wonder what their qualifications are (or any one around them for that matter) to make that permanent determination? I mean I wanted to be a policeman when I was ten and could sit still long enough to think about it. And doesn't this fly in the face of the LGBT argument that people with sexual gender preferences are born that way and it is irrevocable? I agree for the record that there are no doubt genetic tendencies to sexual orientation. Here we have people who clearly aren't "born that way" seeking to reverse engineer biology. The reality Jamie was apparently "born" as a boy. I could understand this with an older child. But to me this strikes me as a form of Eugenics to give the state power to order sex-change proceeders on a 10 year old. When you think about it, what is the difference philosophically between this and some religions forced clitirectomy? Many of those young girls "consent" too? And while many talk about the psychological difficulties of gender mis=identification, what about the difficulties of a boy whose puberty was suspended and then realized later it was just a phase? We're talking about permanent damage to this boys development. While I have no problems with adults seeking their own identity or changing it. Should we allow children unlimited rights to do so? http://www.theage.com.au/national/c...ls-to-solve-the-confusion-20120210-1sjt6.html


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Rebuilding Joplin: Economic Freedom Ruled in Joplin, Missouri
Joplin was struck by an EF5 tornado last May. Afterwards, community members freely and voluntarily worked together to help rebuild the town.
Daniel J. Smith, economics professor at Troy University, studied the rebuilding of Joplin, Missouri in the months following the tornado. Watch as Professor Smith discusses how economic freedom can help areas recover from natural disasters.
"I think one of the key factors in the recovery process in Joplin, from the tornado, is that the government officials allowed the community to start rebuilding itself. I think Joplin is a great example of the power of people—free people—coming together and both using profit motive, in the businesses, using religious reasons for faith-based organizations, and just concern for your fellow man, in the community-based organizations, to rebuild a disaster stricken community." — Daniel J. Smith
Check out http://www.economicfreedom.org/vidoes to see the rest of our videos!
Best part of the video is the fact that the government took a hands off approach!


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The histamine-containing posterior hypothalamic region (PH-TMN) plays a key role in sleep-wake regulation. We investigated rapid changes in glutamate release in the PH-TMN across the sleep-wake cycle with a glutamate biosensor that allows the measurement of glutamate levels at 1- to 4-s resolution. In the PH-TMN, glutamate levels increased in active waking (AW) and rapid eye movement (REM) sleep compared with quiet waking and nonrapid eye movement (NREM) sleep. There was a rapid (0.6 ± 1.8 s) and progressive increase in glutamate levels at REM sleep onset. A reduction in glutamate levels consistently preceded the offset of REM sleep by 8 ± 3 s. Short-duration sleep deprivation resulted in a progressive increase in glutamate levels in the PH-TMN, perifornical-lateral hypothalamus (PF-LH), and cortex. We found that in the PF-LH, glutamate levels took a longer time to return to basal values compared with the time it took for glutamate levels to increase to peak values during AW onset. This is in contrast to other regions we studied in which the return to baseline values after AW was quicker than their rise with waking onset. In summary, we demonstrated an increase in glutamate levels in the PH-TMN with REM/AW onset and a drop in glutamate levels before the offset of REM. High temporal resolution measurement of glutamate levels reveals dynamic changes in release linked to the initiation and termination of REM sleep.
- rapid eye movement sleep
- histamine
- microdialysis
- biosensor
- cortex
various studies have implicated glutamatergic mechanisms in the control of sleep-wake states. In vitro experiments reported a differential glutamate release in brain regions of long-sleep and short-sleep mice (11). Glutamate release was higher during wakefulness than during sleep in the pedunculopontine tegmental nucleus (22), whereas enhanced glutamate release during rapid eye movement (REM) sleep was observed in the rostromedial medulla (24). Paradoxical sleep deprivation increased the content of glutamate and glutamine in the rat cerebral cortex (3).
Glutamate excites both cortical and subcortical neurons and enhances the in vivo release of histamine (HA) through presynaptic N-methyl-d-aspartate receptors in the anterior hypothalamus of the rat (32). Single cell recording and microdialysis experiments demonstrate that HA cell activity is reduced in nonrapid eye movement (NREM) sleep and REM sleep compared with waking (7, 20). We hypothesized that changes in glutamate release in the posterior hypothalamus histaminergic tuberomammillary nucleus (PH-TMN) and in the terminal regions of HA neurons could affect HA release and sleep-wake states. Dysfunction of the Hcrt system produces the sleep disorder narcolepsy (35, 38, 44). Hcrt neurons contain glutamate as a cotransmitter (1). Hcrt effects on sleep-wake state distribution are to some extent mediated by the HA system (17).
The short duration of sleep-wake transition and sleep-wake states makes it difficult to accurately measure the time course of transmitter release across each state using the standard microdialysis-HPLC technique, where samples are collected over a 3- to 5-min interval. In the present study, we used a newly developed glutamate sensor to measure changes in glutamate levels across sleep-wake states with a temporal resolution of 3–5 s (16). We monitored glutamate levels across the sleep-wake cycle in the PH-TMN and compared it with changes in the perifornical-lateral hypothalamus (PF-LH) and cortical areas in freely moving rats. A preliminary presentation of the data has been made (21).
Male Sprague-Dawley rats weighing between 300 and 400 g were used for this study. All procedures were done in accordance with the National Research Council Guide for the Care and Use of Laboratory Animals. Animal protocols were approved by the Institutional Animal Care and Use Committee (IACUC) of the University of California at Los Angeles and by the IACUC of the Veterans Administration Greater Los Angeles Health Care System. The rats were kept on 12h:12-h light-dark cycle (6:00 A.M. lights on, 6:00 P.M. lights off), ambient temperature 24 ± 1°C, with food and water available ad libitum. Rats were anesthetized with ketamine-xylazine (80:10 mg/kg ip). Electrodes for the assessment of sleep-wake parameters were chronically implanted under aseptic conditions, as described previously (18). In brief, bilateral stainless steel screw electrodes were threaded through the skull over the frontal and parietal cortex to record electroencephalogram (EEG). One screw electrode threaded through the midline of the frontal bone was used as ground. Teflon-coated multistranded stainless steel wires with 2 mm exposed at the tips (Cooner Wire, Chatsworth, CA) were placed in the dorsal neck muscles to record electromyogram (EMG). Guide cannulas with stylets (MD-2250; Bioanalytical System) were implanted 2 mm dorsal to the targets in the PH-TMN (A −4.2, L 1.7, H 8.9 mm ventral to dura); PF-LH (A −3.2, L 1.3, H 7.5 mm ventral to dura), and frontal cortex (A 1.2, L 2.5, H 2 mm ventral to dura) for subsequent placement of glutamate sensors (33).
Glutamate sensor data collection.
After surgery (1 wk), the rats were habituated to the recording chamber, and sleep-wake states were monitored. A precalibrated glutamate sensor with 1-mm-long active area was inserted through the guide cannula in the PH-TMN, PF-LH, or frontal cortex and fixed firmly to the guide cannula. The sensor was connected to a four-channel potentiostat (model 3104; Pinnacle Technology) using a flexible cable. The potentiostat was then connected to a personal computer using a USB cable. PAL V1.2.6 software was used (Pinnacle Technology) for acquiring sensor data. Data collection started 2 h after insertion of the glutamate sensor in the brain, at which point a stable baseline was observed. Sleep-wake parameters and glutamate levels were recorded simultaneously (from 11:00 A.M. to 6:00 P.M. during the lights on period) in freely moving rats. Data were collected during spontaneous active waking (AW), quiet wake (QW), NREM sleep, REM sleep, and sleep deprivation. Sleep deprivation studies were performed on the second day. We used only sensor readings taken from the first 2 days after implanting the sensor. We found that, beyond the second day, the sensitivity of the sensor dropped substantially in many cases.
An experiment was conducted to compare glutamate changes recorded using the glutamate sensor with glutamate release using microdialysis-HPLC, across sleep-wake states. In three rats, along with the glutamate sensor cannulas (21-gauge guide, nonsteel), cannulas for microdialysis probes (20-gauge guide, stainless steel) were also implanted in the PH-TMN. The microdialysis guide cannula (blocked with a stylet) was implanted 0.4–0.6 mm lateral (center to center) to the glutamate sensor cannula.
Microdialysis protocol.
After 7 days of postoperative recovery, the rats with microdialysis cannulas were habituated to the rodent microdialysis bowl (Bioanalytical Systems, West Lafayette, IN) and to the flexible EEG and EMG recording cables connected to commutators (Plastics One, Roanoke, VA) that were connected to a Grass polygraph. The day before the recording session (16 h before the experiment), the stylets were removed, and a microdialysis probe was placed through the guide cannula. Microdialysis probes (molecular cut-off size of 50 kDa; AI-01 Eicom) with a semipermeable membrane tip length of 1 mm and an outer diameter of 0.22 mm were used. The length of the probe was set so that the glutamate sensor was 0.4–0.6 mm lateral to the semipermeable membrane, and the estimated dialysis field of the probe included the extracellular environment of the glutamate sensor. The microdialysis probe and glutamate sensor were fixed firmly (dental cement) to minimize tissue trauma and to ensure maximum stability of recording. On the day of the experiment, a glutamate sensor was inserted through the guide cannula in the PH-TMN and fixed to the cannula. Next, the adjoining dialysis probe was continuously perfused with artificial cerebrospinal fluid (aCSF; in mM: 145 NaCl, 2.7 KCl, 1.0 MgCl2, 1.2 CaCl2, and 2.0 Na2HPO4, pH 7.4) at a flow rate of 2 μl/min by a microinjection pump (Bioanalytical Systems). The time taken for the aCSF solution to travel from the tube to the tip of the microdialysis probe was previously determined.
Microdialysis and glutamate sensor recordings.
Data collection started 2 h after insertion of the glutamate sensor in the brain when a stable baseline was observed. Microdialysis samples were collected simultaneously at 5-min intervals (10 μl) using a refrigerated fraction collector (Eicom, Kyoto, Japan). Earlier published studies have reported that 2 h of aCSF perfusion is optimal for achieving a stable measurement of neurotransmitter release (19, 20). The polyethylene collection vials were maintained at 5°C during collection and then stored at −80°C until analyzed. The recovery rate of the microdialysis probes for glutamate was 10–14%. A minimum of three microdialysis samples for each sleep-wake episode were collected.
HPLC assay of glutamate.
The concentration of glutamate in the dialysate was detected by HPLC (EP-300; Eicom) with fluorescent detection (excitation/emission = 340/440 nm; Soma S-3350), as described in our prior studies (19, 20, 28). The sample was injected using an autoinjector (ESA 540; ESA, Clemsford, MA). Precolumn derivatization was performed with o
Recording of sleep-wake stages.
Signals for the assessment of different sleep-wake stages (EEG and EMG) were amplified with a Grass model 78E Polygraph (Grass Instruments, Quincy, MA). All recordings were carried out between 11:00 A.M. and 6:00 P.M. during the lights on period. EEG and EMG signals were digitized using a CED 1401 Plus interface and analyzed manually using Spike2 software (Cambridge Electronic Design, Cambridge, UK). Sleep-wake stages were classified based on electrophysiological parameters as previously described (18). In AW, the animal is alert with movements, low-voltage (desynchronized) EEG, increased levels of muscle tone, and frequent eye movements. In QW, the animal shows limited movement and often rests on the ground with low-voltage EEG and low EMG. NREM sleep is characterized by slow wave activity and low EMG (further reduced from QW). REM sleep is characterized by low voltage EEG, muscle atonia, and theta activity.
Glutamate changes with sleep deprivation.
Changes in glutamate levels before, during, and after sleep deprivation were recorded by glutamate sensors placed in the PH-TMN, PF-LH, or cortex. EEG and EMG recordings were also performed in this group of animals. Eleven rats (5 for PH-TMN, 3 for PF-LH, and 3 for cortex) were subjected to sleep deprivation starting at 11:00 A.M. for periods ranging from 20 to 120 min. Sleep deprivation was performed by gentle handling, which includes cage tapping and brushing the fur with a cotton tip applicator each time the animal showed signs of sleepiness. Sleep-wake states were monitored by electrophysiological parameters and visual observation.
Rats were deeply anesthetized with pentobarbital sodium (60 mg/kg), and transcardial perfusion was performed with normal saline followed by 4% buffered paraformaldehyde. After treatment with 30% sucrose in 0.1 M PBS, the brains were cut at 40-μm intervals using a microtome. Cresyl violet staining was done to verify placement of glutamate sensors and dialysis probes.
We used a glutamate sensor (enzyme-based biosensor; Pinnacle Technology) for the measurement of rapid changes in extracellular concentrations of brain glutamate in freely behaving rats. This enzymatic glutamate biosensor [platinum (Pt)-iridium (Ir) electrode] with an integrated Ag/AgCl reference electrode relies on the glutamate oxidase catalyzed conversion of glutamate and O2 to α-ketoglutaric acid and H2O2 (16). The enzymatically produced H2O2 is detected by its oxidation with an applied potential of 600 mV at Pt-Ir electrodes. Electroactive interferants present in the brain that are oxidized at the same working potential are eliminated by means of a passive selective membrane composed of nafion and cellulose acetate by coimmobilization of ascorbic acid oxidase. This sensor allows the measurement of physiological extracellular concentrations of glutamate with high sensitivity at low concentrations (μM). This electrode has sensing cavity dimensions of 180-μm diameter and 1.0 mm length, with sensitivity of >3nA/10 μM glutamate. It has a fast response time (1–4 s) allowing the monitoring of the physiological time course of glutamate release.
Before implanting the glutamate sensor, an in vitro precalibration was performed using glutamate and ascorbic acid. Changes in glutamate levels were recorded as changes in electrical current. A linear response to glutamate over the concentration range of 0–50 μM was observed (Fig. 1). Changes in glutamate levels in the regions we studied were well within the detection limit of the glutamate biosensor. We and other investigators, using various techniques, showed that glutamate levels across different brain regions never exceeded 50 μM in rats (2, 15, 19, 28, 40).
Only those sensors that responded by at least 3 nA/10 μM glutamate and did not respond to ascorbic acid (250 μM) were used for in vivo experiments. A rapid (1–4 s) response of the sensors varying from 3.2 to 5.5 nA/10 μM glutamate was obtained. A postexperiment calibration was performed immediately following removal of the sensor, after the in vivo experiments. Four out of five AW and REM sleep states, across all the brain regions studied, showed consistent state-related changes in glutamate release using the glutamate biosensor.
Recordings of sleep-wake stages with Spike 2 software were started simultaneously with PAL software for recording glutamate changes. Based on the calibration of each sensor (Fig. 1), we converted PAL data (pA) to micromolar concentrations of glutamate during the corresponding sleep-wake states. Six rats were used for PH-TMN and three rats each for cortex and PF-LH. The changes in glutamate levels reported are the means of pooled data from all AW, QW, NREM, and REM states for all rats.
After the completion of the experiment, histological examination of the brain sections verified the location of the glutamate sensors and microdialysis probes in the PH-TMN and glutamate sensors in the PF-LH and frontal cortex (Fig. 2).
The time course of glutamate release was determined as the time taken from the "start" to the "peak" glutamate levels (as shown in Fig. 3). The start is defined as the first time point of glutamate increase (>20 pA) from a stable baseline (<10 pA variation over 20 s). The peak is the point of inflection at the beginning of the plateau (>20 pA variation at consecutive data points over 20 s). The time course of glutamate clearance was determined as the time taken from the "drop" to the "postbasal" glutamate levels. The drop is the first time point of glutamate decrease (>20 pA) at the end of the plateau. The postbasal period is the first time point of glutamate return to a stable postbasal reading lasting at least 20 s. The duration of increased glutamate levels was defined as the time taken from the start to the drop in glutamate levels.
Baseline glutamate concentration was taken as the average of the 20 s before the start of each state-dependent glutamate change. This reduces the effect of any circadian influence and any gradual decline in the sensitivity of the sensor. The highest glutamate concentration was determined as the average values from the peak to the drop in glutamate levels. The increase in glutamate concentration was then calculated as the difference between the highest and the baseline readings.
The latency of glutamate changes relative to the onset of each sleep-wake state was calculated as the time difference between the onset of the state and the start of increased glutamate levels. The latency of glutamate changes relative to the offset of each sleep-wake state was calculated as the time difference between the offset of the state and the drop in glutamate levels.
We observed a marked increase in glutamate levels in the PH-TMN coinciding with the onset of REM sleep compared with NREM sleep (Fig. 3A). The average increase in glutamate concentration in REM sleep was 0.36 ± 0.04 μM above that of the prior NREM sleep period (46 episodes, 6 rats). The start of the increase in glutamate levels was tightly linked (0.6 ± 1.8 s) to the onset of REM episodes (i.e., onset of EEG theta activity and muscle atonia, Figs. 3 and 4). The start of the drop in glutamate levels preceded REM sleep offset by 8.0 ± 3.3 s (Figs. 3 and 4). The magnitude of the increase in glutamate levels was not correlated with the duration of REM sleep. However, there was a high correlation between the duration of increased glutamate levels (from start to drop) and the duration of REM sleep [r = 0.92, degrees of freedom (df) 45, P < 0.0001; Fig. 3B]. The time taken for glutamate levels to fall from peak to basal values (22.4 ± 4.0 s) with REM sleep offset was similar to the time taken for glutamate levels to increase from start to peak values (27.7 ± 4.2 s) with REM sleep onset (Table 1).
Variation in glutamate levels was calculated relative to AW onset and offset (Fig. 5). We observed that glutamate levels started to increase after the onset of AW (5.4 ± 15.7 s) but started to decrease before the offset of AW (47.2 ± 25.6 s). Glutamate levels increased in AW by 0.32 ± 0.05 μM compared with the preceding state. The magnitude of the relative changes in glutamate levels with AW was similar when AW was preceded by either NREM or QW. We did not observe any changes in glutamate levels linked with muscle tone. There was a high correlation between the duration of AW and the duration of increased glutamate levels (r = 0.91, df 16, P < 0.0001; Fig. 6A). The magnitude of increase in glutamate levels was also significantly correlated with the duration of AW (r = 0.63, df 16, P < 0.01; Fig. 6B). The time taken for glutamate levels to reach peak values after onset of an AW period (140.3 ± 40.8 s) was nonsignificantly longer than the time taken for glutamate levels to return to basal values in the subsequent state (89.5 ± 15.8 s; Table 1).
Short periods of sleep deprivation by gentle handling (20–120 min) produced gradual increases in glutamate levels in the PH-TMN. Glutamate sensor data showed that glutamate levels peaked 15–20 min after the initiation of sleep deprivation (forced waking). Glutamate levels increased up to 1.51 μM from basal values. Termination of sleep deprivation led to a gradual reduction in glutamate levels. Spontaneous waking increased glutamate levels by 0.32 μM.
Glutamate levels in microdialysis samples collected during REM sleep were higher than those collected during AW and NREM sleep (AW = 2.3 ± 0.12; NREM = 2.4 ± 0.06, REM = 2.5 ± 0.17 pmol/sample). However, these differences were not statistically significant. Microdialysis samples from the PH-TMN also showed a nonsignificant increase in glutamate levels with sleep deprivation compared with spontaneous waking (2.8 ± 0.02 vs. 2.5 ± 0.04 pmol/sample). These results are consistent with results obtained with the glutamate biosensor, although they lack its temporal resolution (Fig. 7).
The highest glutamate levels in the PF-LH were observed during AW compared with NREM sleep (27 episodes from 3 rats; Fig. 8A), as in the PH-TMN. There was a high correlation between AW duration and the duration of increased glutamate levels (r = 0.91, df 26, P < 0.0001; Fig. 8B). The time taken for glutamate levels to decrease at the offset of AW was significantly longer than the time taken for it to increase at the onset of AW (16.7 ± 3.8 vs. 8.6 ± 1.3 s, t = 2.0, df 54, P < 0.05; Table 1).
Glutamate levels increased in REM sleep (by 0.42 ± 0.09 μM) compared with the prior NREM sleep periods. This was also observed in the PH-TMN. Sleep deprivation produced a nonsignificant increase in glutamate levels compared with spontaneous AW (0.50 ± 0.08 μM with sleep deprivation vs. 0.52 ± 0.05 μM in AW).
Frontal cortex.
Glutamate levels in the frontal cortex increased with AW (16 episodes) and REM sleep (16 episodes) compared with NREM sleep (from 3 rats; Fig. 9A). Similar findings were observed in the PH-TMN and PF-LH. There was a significant correlation between AW duration and the duration of increased glutamate levels (r = 0.67, df 15, P < 0.01; Fig. 9B). Sleep deprivation increased glutamate levels significantly more than spontaneous AW [0.72 ± 0.14 μM with sleep deprivation vs. 0.35 ± 0.05 μM in AW; t = 3.0, df 21, P < 0.007]. REM sleep duration was also significantly correlated with the duration of increased glutamate levels (r = 0.65, df 15, P < 0.01). The time taken for glutamate levels to increase with AW was significantly longer than the time taken for glutamate levels to decrease to basal levels (120.6 ± 21.0 vs. 68.1 ± 12.3 s; t = 2.2, df 30, P < 0.03; Table 1). This was also the case in REM sleep (42.4 ± 6.6 vs. 20.3 ± 3.5 s; t = 3.0, df 32, P < 0.005; Table 1).
The time taken for glutamate levels to increase from "start to peak" and to decrease from "drop to baseline" was faster in the PF-LH compared with both the PH-TMN and the frontal cortex. Furthermore, glutamate levels increased at a faster rate than it decreased during REM/AW onset and offset in the PF-LH. This is in contrast to the faster decrease in glutamate levels compared with its increase in the PH-TMN and frontal cortex (Table 1).
Analysis of variance of the changes in glutamate levels and of the time course of glutamate variation at REM sleep onset (20 s before and 20 s after REM onset in 5-s periods) showed a significant difference in glutamate levels across the three brain regions [F(2,92) = 9.2, P < 0.0001, ANOVA]. There was also a significant effect of time course on glutamate levels [F(7,322)=40.8, P < 0.0001, ANOVA] and the interaction of these two variables [F(14,644) = 9.6, P < 0.0001, ANOVA]. On the other hand, at REM sleep offset (30 s before and 15 s after the REM offset), glutamate levels did not differ significantly across the three brain regions. The effect of time course on glutamate levels [F(8,368) = 30.3, P < 0.0001, ANOVA] and the interaction of these two variables [F(16,736) = 7.7, P < 0.0001, ANOVA], however, were significant.
Analysis of variance of the changes in glutamate levels at AW onset showed there was no significant difference in glutamate levels (20 s before and 20 s after the AW onset) across the different brain regions. However, there were significant effects of time on glutamate levels [F(7, 231) = 7.2, P < 0.0001, ANOVA] and a significant interaction of these two variables [F(14, 462) = 2.8, P < 0.0006, ANOVA]. In contrast, AW offset (30 s before and 15 s after the AW offset) showed no significant difference in glutamate levels across brain regions. However, there were significant effects of time on glutamate levels [F(8,256) = 10.2, P < 0.0001, ANOVA] and a signifcant interaction of these two variables [F(16,512) = 1.6, P < 0.05, ANOVA].
We observed increased glutamate levels with AW and REM sleep compared with NREM sleep. The increase in glutamate levels strongly coincided with REM sleep onset (0.6 ± 1.8 s) and less strongly with AW onset (5.4 ± 15.7 s) in the PH-TMN. Decreased glutamate levels preceded the offset of AW and REM sleep. These findings suggest that processes linked to reduced glutamate levels may be involved in the termination of AW and REM sleep states.
Glutamate is not enzymatically broken down in the synaptic cleft; however, evidence suggests that most free glutamate is cleared from the cleft very rapidly (10, 47), perhaps within 1 ms (6). In theory, such rapid clearance might be accomplished by diffusion alone (49). However, a study by Tong and Jahr (45) suggested that binding to glutamate transporters speeds the clearance of free glutamate. This rapid turnover of glutamate may not be detectable by the standard microdialysis-HPLC techniques, which require much longer duration samples.
Simultaneous glutamate measurements by microdialysis and by the glutamate biosensor were recorded in the PH-TMN. Consistent with the findings of Nitz and Siegel (28), we did not observe any significant variation in glutamate levels across sleep-wake states using the microdialysis technique. This lack of state-related glutamate change could be due to the greater temporal and spatial resolution of the glutamate biosensor compared with the microdialysis technique. This study demonstrates for the first time an increased release of glutamate with REM sleep onset and a decreased release of glutamate before the offset of REM sleep in the PH-TMN. These changes would not have been observable with microdialysis measurement, because the REM duration (1–3 min) in rats is shorter than the normal microdialysis sample collection period (3–5 min).
Hu et al. (16) reported that the glutamate sensor responded to glutamate with a much higher selectivity compared with other interferents, including neurotransmitters [dopamine, norepinephrine, serotonin, γ-aminobutyric acid (GABA)], various metabolites (3,4-dihydrophenyl acetic acid; 4-hydroxy-3-methoxyphenylacetic acid, 3-methoxy-4-hydroxy-phenylglycol, and 5-hydroxyindolacetic acid), and other endogenous electroactive species (l-tyrosine, l-cysteine, l-tryptophan, and l-glutathione). They also showed that there was little or no immediate response when these interferents were added to PBS to mimic in vivo extracellular fluid concentration. Hu et al. (16) went on to show that local microinjections of exogenously applied glutamate in the dentate gyrus of the rat hippocampus, adjacent to the sensor, resulted in an immediate increase in glutamate sensor readings that peaked within seconds of the application. These authors also showed that local application of potassium chloride solution resulted in increased hippocampal glutamate levels as measured by this sensor. Also, electrical stimulation of the perforant (glutamatergic) pathway consistently elicited a peak glutamate sensor reading, whereas a "blank" electrode (identical to the glutamate sensor except without glutamate oxidase) located adjacent to the glutamate electrode showed no change in response to the electrical stimulation of the perforant pathway. These findings demonstrate the selectivity and specificity of the glutamate biosensor in vitro as well as in vivo.
The activity of HA cells of the PH-TMN is highest in waking and lowest in REM sleep (20, 43, 48). We found high glutamate levels in the PH-TMN during both AW and REM sleep compared with NREM sleep. Recent work showed that simultaneous saporin-induced lesions of the HA-, acetylcholine-, and norepinephrine-containing neurons had little effect on the duration of waking (4). The present results suggest that widespread glutamate release may be sufficient to mediate waking, even in the absence of these cell populations. In the intact animal, glutamate release is likely to have a major role in activating these wake-promoting cell groups.
The PH-TMN receives glutamatergic afferent projections from the prefrontal cortex, lateral preoptic area, and lateral hypothalamus (5, 13, 46, 50). Glutamatergic projections may directly activate PH-TMN histaminergic neurons. Hypocretin neurons densely innervate the soma and proximal dendrites of the TMN cells (6). Torrealba et al. (46) showed colocalization of Hcrt and glutamate in axon terminals in the TMN in rats. Most of the Hcrt-immunoreactive terminals in the PH-TMN are glutamatergic and form typical asymmetric, excitatory synapses primarily on the cell bodies and proximal dendrites of PH-TMN neurons (46). The proximity of the glutamatergic vesicles to the synaptic complex suggests that, when these PF-LH neurons fire at low frequency, glutamate neurotransmission should predominate. However, when they fire at higher frequency, the additional release of Hcrt from nonjunctional dense-core vesicles would presumably reinforce the excitation (46). Hcrt exerts a wake-promoting effect through the histaminergic system (17). The effect of Hcrt-1 in waking is linked to glutamate release from the locus coeruleus and the motor nucleus of the trigeminal in rats (23, 34). Hcrt produces a calcium-dependent glutamate release in certain nuclei of the central nervous system (19).
Glutamate may also modulate the activity of HA neurons through its interaction with other wake-related monoaminergic systems. The PH-TMN receives afferent projections from monoaminergic inputs, originating from the adrenergic, noradrenergic, and serotonergic cell groups of various brain regions (12). The PH-TMN neurons also receive an ascending, presumed cholinergic input from the mesopontine tegmentum (13) that is important in brain arousal mechanisms.
Our findings suggest that the changes in HA cell activity during REM sleep are not a consequence of reduced glutamate release. Rather, like the locus coeruleus and the raphe cells, which are silent in REM sleep, HA cells may be actively inhibited during sleep (14, 28, 29, 30). We hypothesize that glutamate released during REM sleep may activate GABAergic interneurons within target areas as well as GABAergic projection neurons, thus inhibiting HA cells in the PH-TMN. Moreover, PH-TMN neurons receive strong GABAergic inputs from the diagonal band of Broca, lateral hypothalamus, and the preoptic and ventrolateral preoptic regions (36, 37, 41, 51). GABA released from these sites can inhibit TMN neurons by acting on both GABAA and GABAB receptors (42, 51). Galanin, which is colocalized with GABA from preoptic projection neurons, may also contribute to the inhibition of HA neurons during REM sleep (37). Increased GABA release in the PH has been reported during REM sleep (28). Nishibori et al. (27) and Oishi et al. (31) reported that GABA agonists decreased the turnover of HA in mouse brain. These findings suggest that increased levels of GABA may override any direct effects of glutamate on HA neurons during REM sleep.
Increased glutamate levels during AW and REM sleep were also seen in the cortex. A recent report using microdialysis also demonstrated an increase in the concentration of glutamate in the rat orbitofrontal cortex during REM sleep (26). We also found increased glutamate levels during AW and REM sleep in the PF-LH. PF-LH Hcrt neurons are involved in the regulation of sleep-wake function (9, 38, 39). Li et al. (25) showed that Hcrt-mediated excitation of local glutamatergic neurons can increase Hcrt neuronal activity, in part by presynaptic facilitation of glutamate release. We found that, in the PF-LH, glutamate levels took a longer time to return to basal values compared with the time it took for glutamate levels to increase to peak values during AW. This is in contrast to the other regions we studied (PH-TMN and frontal cortex) in which the return to basal values at AW offset was quicker than their rise with AW onset. This suggests the possibility of a less robust glutamate clearance mechanism in the PF-LH compared with the PH-TMN and the cortex.
Perspectives and Significance
This study provides evidence of rapid increases in glutamate levels with REM sleep and AW in the PH-TMN, PF-LH, and frontal cortex. The glutamate biosensor is superior to the standard microdialysis-HPLC technique in providing the temporal resolution required for detection and description of sleep-wake-related changes in glutamate concentrations.
Funding for this study was provided by Grants HL-41370 and MH-64109 and by the Medical Research Services of Department of Veterans Affairs.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
- Copyright © 2008 the American Physiological Society


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On Tuesday, I met with Vanessa Williams to talk about her recent Emmy nomination for Ugly Betty, fish pedicures, and Botox. Vanessa, who has always been very open about her use of the wrinkle-fighting drug, is currently making a few stops throughout the country for the Botox Cosmetic: Express Success Campaign, an educational tour that benefits the Dress For Success organization.
Have you ever wondered why Vanessa took the leap and admitted she uses Botox, or how it affects her ability to act? Find the answers and learn about some of her unexpected hobbies after the jump.
Tell me how you got involved with Botox in the first place, and the Dress For Success campaign.
Allergan [maker of Botox] approached me with the idea. They told me how they had teamed up with Dress For Success, and I jumped on board. I think I've been candid about my use with Botox Cosmetic since I started the show three years ago. In the pilot, I get Botox from my assistant in Ugly Betty; journalists had asked if I had ever used it, and I've been very candid about my use . . . It was the perfect combination of being able to be vocal, educating women about the product, but also giving back, and Allergan gave $250,000 to Dress For Success so they can help a nonprofit. It's kind of a win-win situation.
Does it hurt?
It depends on the practitioner. My doctor is very quick and is masterful with his hands. And you want to go to somebody who knows what they're doing as well, and make sure you're getting Botox Cosmetic, too, because there have been lots of bad [off-label] experiences.
What made you decide to be so honest about using Botox? There are so many actresses that you can tell use it, but they don't admit to it.
I don't know why you would lie about something if someone asks you a question. I don't know why they would not tell the truth . . . But also, I use it sparingly, too, so I have expression. I've been lucky enough to be nominated for three Emmys . . . So, obviously I can continue to move and have expression and do my job well.
What's something that people don't know about you?
People are surprised when they find out about my love of cars. I have a bunch of cars, I love driving and I love driving fast — always under the speed limit! I listen to Irish music on Saturday mornings on WFUV. My kids find that torturous, but I subject them to it because I love it. I ride horses and I collect horses, statues, paintings, and pictures. I bake carrot cakes for my friends for their birthdays.
With cream cheese frosting?
Of course, I get a few requests and do that with love.
But wait, there's more! Come back tomorrow for more of my interview with Vanessa.


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By gandreas software
This app is only available on the App Store for iOS devices.
A favorite on college Unix systems in the early to mid-1980s, Rogue popularized the dungeon crawling computer game dating back from 1980 (and spawned entire class of derivatives known collectively as "roguelikes"). gandreas software now presents the classic for the iPhone/iPod Touch:
- Playable in either "ASCII" mode, or graphics mode (just rotate the device to switch)
- Obscure keyboard commands replaced with a simple taps for movement, or a handy command picker.
- Commands can also be activated by a unique gesture based command - want to search for a secret door? Swipe across the top of the play area (all the gestures are shown on the command picker for easy reference)
- Graphics can be zoomed in/out via pinch
- Completely faithful Rogue experience (all the levels, monsters, potions, scrolls, etc...)
Explore the Dungeons of Doom and retrieve the Amulet of Yendor, or die trying!
iPhone Screenshots
Customer Reviews
Perfect little 'casual' dungeon crawl game.
There is a reason why Rogue is a classic, and I'm still able to enjoy myself 23 years after I first saw it. I was even playing this on my PC less than ten years ago while waiting for a download to complete. Sure there are more advanced clones of this (Nethack, Larn, Moria, etc..), but Rogue excelled with the simplisticness. I was hesitant over the touch interface, but actually I warmed up to it after a few games. (In fairness, the somewhat obscure keyboard method wasn't much better on PC's, but it was all we had.) I'm embarrassed to say that my largest complaint was simply that it may not be a great fit for the itouch. The screen is just a little too small to play without eye strain, and a zoom feature would make this much more comfortable to play, even though when I've had it on other versions (like for the Atari ST), I always needed to keep zooming out in order to see the whole map in order to figure out which direction to go in next. However, I say 'was going to be a complaint' because I played it several times without realizing that if I rotated the screen, the game automatically zoomed into a well drawn and playable closeup. Very nice. It may feel a little old school to some, but it is definitely well worth the playtime.
Excellent idea, but could use improvement
1. As others have mentioned, there is a throwing bug where it throws something other than the intended item. 2. The response to transition between portrait and landscape view when the screen is rotated is slow and sometimes doesn't respond at all. 3. Pitch zoom is fine for photos, but terrible for games. Would suggesting using a two finger/three finger tap gesture for zoom in/out. 4. Does each character icon have different stats/characteristics/item specific luck? It seems that the only change is the icon. 5. The embbedded faq mentions the importance of saving the game, but I didn't figure out how to do this. Seldom if I close the app I can pick up where I left off, more often it starts a new game. 6. Difficulty selection would be nice. 7. Please consider a port of Larn or uLarn. It's more diverse than Rogue and much more entertaining.
classic dungeon crawl fun!
Evolutionally speaking, Rogue is that fish with leg-like appendages that first walked upon land - a direct ancestor of Diablo and World of Warcraft. The graphics mode is a nice touch to keep it fresh for modern audiences, though I prefer ASCII mode. While there is definitely room for improvement and simplification of the game, I'm sure gandreas software did everything it could within licensing limitations - this is a port, after all. Rogue's difficulty reflects a realism that most of today's games lack. When you die, you're dead - start over from scratch. Everything is working against you. Only a combination of your wits, good planning, and extraordinary luck will see you through to a winning game. I've never won, and I'm not sure I ever will. But God help me, I can't get enough of it.
- Free
- Category: Games
- Released: Nov 28, 2008
- Version: 1.0
- Size: 0.4 MB
- Language: English
- Seller: Glenn Andreas
- © 2008 gandreas software
Compatibility: Requires iOS 2.1 or later. Compatible with iPhone, iPad, and iPod touch.


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Spain's top investigating judge Baltasar Garzon is to probe suspected torture and ill-treatment of inmates at the US prison of Guantanamo Bay, the daily El Pais has reported.
The paper reported that Judge Garzon would be acting on complaints lodged by a number of associations, focussing on one prisoner, Ahmed Abderraman Hamed, who has Spanish nationality.
Three other detainees, Moroccan Lahcen Ikasrrien, Palestinian Jamiel Abdulatif al-Banna and Libyan Omar Deghayes would also be concerned as they had links with Spain, El Pais said.
In 2005, Spain declared itself competent to investigate any crime committed abroad, but after diplomatic problems the scope of the inquiries was reduced in 2009.
Spanish courts can now deal only with cases that have a clear link with Spain, or cases that are not being investigated in countries where the offences are alleged to have been committed.
El Pais said Washington had not replied to a request made seven months ago from Madrid as to whether it was investigating the allegations now being taken up by Garzon.
The Palestinian Authority's foreign minister Riyad al Malky said in Madrid last week that Spain had agreed to accept a Palestinian Guantanamo Bay detainee.
The unnamed man will be transferred to Spain in early February along with another man whose nationality has not been confirmed, according to press reports quoting Spanish diplomatic sources.
US President Barack Obama has promised to close the controversial prison camp for terror suspects in a US enclave on Cuba, and the United States has started to slowly empty it of detainees.


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Mudcats stop Grand Rapids 3-1
The Bemidji Mudcats took another step forward in Arrowhead League play Wednesday night, stopping the Itasca Indians of Grand Rapids 3-1 at BSU.
It lifted the Mudcats to 5-0 in league play and dropped the Indians to 1-2. Overall Bemidji is 10-2.
The Cats will host the Blue Ox tonight at 7 in a non-league game and entertain the Duluth Xpress in a 1 p.m. twin bill Saturday.
The Xpress was 2-0 at last report but has likely played more games.
Paul Fenner, who hurled a one-hitter last week in a 3-2 win at Nashwauk, carried a no-hitter into the seventh Wednesday and settled for a four-hit win.
He fanned eight and walked none in a snappy 1:43 game.
Tyler Blomberg was almost as strong through four frames, allowing no hits.
But in the fifth, Doug Peterson tripled with one gone, a sinking line drive that just eluded center fielder Ryan Graupman's diving grasp.
Simon Anderson followed with a topper down the third base line that barely stayed fair in its 20 foot path, giving him a rare infield single as Peterson scored.
Andrew Hengel then hit a comebacker to the mound which Blomberg threw into center field as Anderson reached third.
He scored on Dan Bauer's sacrifice fly.
Tony Klaers then singled up the middle to score Hengel.
The Cats had one other threat with Bauer and Klaers getting back-to-back singles with two gone in the seventh. But Dan Nolan forced Klaers at second to end that threat.
Manager Jim Brubaker worked a scoreless eighth.
The pair struck out eight and walked three,
Grand Rapids ended the no-hitter and shutout in the seventh when Sam Sparen singled, stole second and scored on Jason Hron's one-bagger.
The Indians had singles in the eighth and ninth but stranded both runners at first.
Fenner reached 3-0 on the year.
Brian Murphy is a likely starter tonight with Peterson and Tyler Norland expected to be available for Saturday's twin bill. Norland has not pitched since the season opener at Nimrod.
If Norland is not available, Murphy will probably be saved for the Xpress.
The Cats shaded the Blue Ox 3-2 in their first meeting.
Grand Rapids 000 000 100 - 1 4 3
Mudcats 000 030 00x - 3 6 0
Blomberg (1-1) l, Brubaker (8) and Brubaker, Dorholt (8)
Fenner (3-0) and Klaers


text:
SALT LAKE CITY — Schiff Nutrition International on Wednesday named Shane Durkee SVP research and development.
"We welcome Shane and believe his proven track record in driving nutritional supplements innovation will contribute significantly to accelerating our new product program and organic growth," Schiff president and CEO Tarang Amin said.
Durkee, 39, has more than 16 years of consumer products research and development experience in leading teams in innovation, product development and medical science. Most recently, he was the director, global innovation and new technology at Bayer Consumer Care in Basel, Switzerland. In this position, he led product innovation and development within the nutritional, dermatologic and gastrointestinal business units, which had more than $2.7 billion in annual sales. He also served in R&D leadership roles working on Bayer's U.S. branded nutritional business, including One-A-Day, Flintstones and CitraCal. Prior to joining Bayer, Durkee held R&D leadership roles with TwinLab and Nutraceutical Corp.
Durkee holds a B.S. in Microbiology and an M.B.A. He has served as a member of the Senior Scientific Advisory Council for the Council for Responsible Nutrition and as a science advisory board member at Virgo Publishing.
Interested in this topic? Sign up for our weekly Retail Health Provider e-newsletter.


text:
So here we are, just three(ish) months away from 26.2 miles through our nation's Capitol. And let's just say my training is off to a, uhhh, bumpy start. The RW Run Streak got me hopped up on speed and strength, which helped me run a post-college 5K PR of 19:42 (and snag a top overall female win!) at a race my old teammate puts on in honor of her mother last weekend. I've also been consistently hitting the gym two to three times a week, and I'm already feeling stronger head-to-toe. (And get this, I figured out how to enjoy planks, even the dreaded side planks! Rather that holding a position until my core gives out, I'm rotating positions every 20 seconds, doing at least three sets per gym session. Plus, according to my roomie, shorter bursts are better because you're more likely to hold proper form. Rock hard abs, here I come!)
But...that momentum came to a screeching halt when I went on vacation with my family last week. I did one glorious run with my Dad on the beach (that's him above - he's training for the RW Half!), but that was it. I'll be honest, whenever I'm with my family, running goes on the back-burner. I hardly ever see them, so the time is precious. I'd rather be with them than on the roads alone. I've got 50 other weeks to do that. As much as I needed to hit the mental reset button, I'm ready to dive right back in to training. Taking a week off from the get-go has left me a bit anxious, but I know that my off-season streak and newfound need to lift stuff has given me a solid base. Since strict day-by-day plans are still the bane of my existence, I'm going to keep up my flexible routine. Here's a rundown of my goals and what I'm hoping to do training-wise:
- This race marks just over a year anniversary since my first marathon. I haven't run as fast since, so I'd be thrilled with a PR. Don't care by how much, but you know, deep down I'd love to cross the line in the low 3:2X's.
- Speaking of that uber-successful first marathon, I went through my training log and wrote down what I did for my long runs leading up to Steamtown. The goal is to more or less copy that progression since it worked so well last time. Don't fix what ain't broken, right?
- Ideally I'd like to do some sort of speed session once per week, because I finally got the itch to do genuine workouts. It took a year, but the desire has returned. Whether it's doing Wednesday intervals at work or throwing a tempo run into the mix, upping my turnover to offset those long, slow distance runs will hopefully make me faster come October.
- No excuses, I'm going to lift at least twice a week. A third time and/or yoga is a bonus.
- I trained through the heat last year and it paid off. Every time I want to skip out on a run because of the sauna-like conditions, I'll wipe the sweat out of my eyes and focus on that fact. Yes, summer running sucks, but remembering that it's only going to get cooler will make those miserable miles worthwhile. And hey, maybe that's why I ran as fast as I did at Steamtown!
Long story short, my weekly routine should look like this: 1 long run + 2-3 lifting sessions + 1 speed workout - any heat-related excuses = a successful Marine Corps Marathon!


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Public servants must remember who they serve
Sussex County Planning and Zoning Commission is considering a proposal to rezone a 38-acre parcel along Route 24 from agricultural-residential to medium-density residential planned community. That means instead of two units per acre, if the zoning change is approved, the developer could build 3.3 units per acre.
That was not good news for a man who lives in the area and is aware of traffic problems on Route 24. In carefully proposed testimony during a recent hearing on the proposed zone change, he put the issue succinctly: "I'm not against development in the area, but I'm against a change of zoning that allows for more units, compounding traffic problems on Route 24," he said. He also called for a broader infrastructure plan to support future development in the area.
The citizen's remarks are reasonable – and right in line with the thinking of many Cape Region residents. But his testimony drew only sarcasm, with one planner blaming the region's traffic problems on state transportation officials.
It's time for county planners to realize that ploy just doesn't work anymore.
Planning officials and county council, not DelDOT, are responsible for land-use decisions. It is quite simply irrational for county officials to expect DelDOT to build roads anywhere council decides to allow development.
As our region becomes ever more congested, county planners and council have two choices: say no to further development, or like other jurisdictions nationwide, say yes to development but require developers to fund the necessary road and traffic improvements as a condition of approving the projects.
Sussex County's two-unit-per-acre zoning is already the least restrictive zoning in any county on the Delmarva Peninsula. Changing zoning to allow even more units – without proper infrastructure – is misguided.
Even more misguided is questioning the insight of citizens who take part in the landuse planning process. Council is elected and planners are appointed to serve and listen to the people of Sussex County, not to quiz them on the nuances of state and local government.
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|18 Feb 2014
Install error MS Office2003 compatibility pack error
Office on-line suggested posting here. I can't install compatibility pack for office '03. I get an error accessing registry key UNKNOWN\component\DA42BC89BF25FD0AF etc. No such key found with Registrar. Tried clean boot,run as administrator,runassystem.exe-FileFormatConverterss.exe with same result. Thank you in advance for any help.
|My System Specs
|18 Feb 2014
Have you checked out this MS website. It may provide some help for you.
How to install the Microsoft Office Compatibility Pack so that you can open and save Office Open XML formats in earlier versions of Microsoft Office
|My System Specs
|20 Feb 2014
I couldn't find any real help there. I should have mentioned though I had office 2003 previously installed with compatibility pack. After uninstalling it I used MS Fixit utilities for removing Office '03, 07, and 2010 followed by several different registry cleaner scans.
|My System Specs
|20 Feb 2014
Do you have itunes installed. If you do then this website may help as there is reference to your UNKNOWN registry error.
|My System Specs
|22 Feb 2014
I'm almost certain that was the problem, but I had already done a Win 7 repair install. (I waited to long to use System restore and the restore points were to recent. The first thing I was required to do before the Windows install would run is UN-install iTunes.
|My System Specs
|22 Feb 2014
At least you have it repaired even though you ended up doing a reinstall.
|My System Specs
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