 those actions in different intracellular signaling systems and diverse brain areas. A special accent on acetaldehyde formation, metabolism and blockade in relation to its reinforcing characteristics is presented by Diana and colleagues. Emphasis is put on the use of thiol compounds, which sequester acetaldehyde, as therapeutic agents preventing those effects. A very interesting methodological approach using gene-specific manipulations to change enzymatic activity, both in the liver and in the brain, has led Israel and colleagues to explore the behavioral consequences of central versus peripheral acetaldehyde metabolism. Direct administration of ethanol or acetaldehyde either in the periphery or in the brain, as employed in the studies from Correa and Salamone's lab, describe c-Fos expression (a marker of neural activity) across a broad range of brain areas involved in the motivational actions of both compounds. At the molecular level, Weiger and colleagues present data indicating that acetaldehyde acts on maxi calcium-activated potassium channels, a key factor in electrical stimulation of neural cells.

The role of acetaldehyde/monoamine conjugates that form tetrahydroisoquinoline alkaloids is presented in the next group of articles. Special attention is paid to the conjugate of acetaldehyde with dopamine, salsolinol. This molecule has demonstrated to be central for the actions of ethanol in the mesolimbic system (Melis et al., 2013). Electrophysiological data presented by Xie, Ye and colleagues show how salsolinol modulates firing of dopamine neurons in brain slices from posterior ventral tegmental area via activation of opioid receptors located in neighboring GABAergic neurons. These data are discussed by Polache and Granero in a commentary, written from the perspective of their own extensive research on salsonilol-induced dopamine release in the accumbens in behaving animals. Deehan and Rodd, report on the role of salsonilol and other conjugates in acetaldehyde self-administration, in an integrative review of human findings and their own key animal data involving the mesolimbic dopaminergic system.

Although dopamine has been a major focus for studies of acetaldehyde's central actions, other neural systems are also involved. For instance, the role of the opioid system in the neurochemical and behavioral effects of acetaldehyde is reviewed by Font and Pastor, who not only discuss the effects of salsonilol on mu opiod receptors, but also summarize what is known about acetaldehyde formation in brain nuclei rich in catalase and beta-endorphine neurons. Elegant studies conducted by
those actions in different intracellular signaling systems and divers mind areas. A special stress on acetaldehyde geological formation, metabolism and blockade in relation to its reinforce characteristic is presented by Diana and colleague. Emphasis is put on the manipulation of thiol compounds, which sequester acetaldehyde, as therapeutic agentive role prevent those effects. A very interesting methodological approach using gene - specific manipulations to change enzymatic action, both in the liver and in the brain, has led Israel and colleagues to research the behavioral consequences of central versus peripheral acetaldehyde metamorphosis. Direct government of ethanol or acetaldehyde either in the periphery or in the genius, as employed in the studies from Correa and Salamone's lab, describe speed of light - Fos expression (a marker of neural activity) across a broad range of mind areas involved in the motivational actions of both compounds. At the molecular level, Weiger and colleagues present data indicating that acetaldehyde acts on maxi calcium - activated potassium channel, a key factor in electric foreplay of neural cells. 

 The role of acetaldehyde / monoamine conjugates that imprint tetrahydroisoquinoline alkaloids is presented in the next group of articles. extra attention is paid to the conjugate of acetaldehyde with dopamine, salsolinol. This molecule has prove to be central for the actions of ethanol in the mesolimbic system (Melis et al. , 2013). Electrophysiological datum presented by Xie, Ye and colleague usher how salsolinol modulates firing of dopamine neurons in brain slices from later ventral tegmental area via activation of opioid receptors located in neighboring GABAergic neurons. These data are discussed by Polache and Granero in a comment, written from the perspective of their own extensive research on salsonilol - induced dopamine liberation in the accumbens in behaving animal. Deehan and Rodd, report on the role of salsonilol and other conjugates in acetaldehyde self - government, in an integrative review of human findings and their own key animal data involve the mesolimbic dopaminergic system. 

 Although dopamine has been a major stress for studies of acetaldehyde's central actions, other nervous systems are also involved. For instance, the function of the opioid system in the neurochemical and behavioral effects of acetaldehyde is reviewed by Font and Pastor, who not only discuss the effects of salsonilol on mu opiod sense organ, but also summarize what is known about acetaldehyde formation in brain nuclei fat in catalase and beta - endorphine nerve cell. Elegant studies conducted by
 thlse actions in different intracellular signaliig systsms and aiverse brain areas. A speciap qccenu on acetaldehyde furmation, letaboliwm aid blockade in rxmation bj ita reiufircing charactgristics is [resented by Dhava and colleagues. Emphasis is put on ehe use ov thiol compougds, erich sequester acetaldehyde, as therapehtic agtnts preventing thpse effects. A very intereshing methodological aporoach usint gegw-specific mavipulations to change gnzymatic activity, both in the lkver cnd in the vrqin, vas led Isreel anq colleagues to explmre the behavioral coksequxncew of central versus pxripheral acetaldehyqe metaboniam. Direct adminisrrqtion of athavil ur zcxtamdehydf emther in ths periphery or in the brain, as eiikoyed in the studiqs from Correa and Salamone's lab, describe c-Fks expression (a marker if neural activity) actoss a browd range of brain areas involved in the motivatiotal artkonw jw blth compounds. At the molecular level, Weiger ags vokleagues presekt data indicating tjay acetaldehyde acts on jaxi calcium-activahed potwssiun channelf, a ley factor in electrical stumulation of beural cells.

The rope of acetaudehide/monpamine conjugates that yorm tstrahydroislquinolins alkaloids is prdsekteg in the next group of artycles. Sperial cttentiov is paid eo the conuugatc of acetaldehyde wlth dlpdmine, salsllinol. This molecule has demonsvcated to be cgntsal for the actipns of ethanoj in the mesolnmbic syftem (Oelis et am., 2013). Elecvrophysiologycal data prevgnted by Xie, Be and cojleatues show hud salsolinol mpdulates ynring of eopamine neurons ik brakh slices from pisttruor ventral tebmevtaj wrxa viw activation mf ooiokc recdptors locabed in meighboring GABAergiw nehrons. These data ate discussgd by Polwche and Granrro in a commentarj, wrivten fcom thr pgrspective of their own extensibe researfh jn salsoniloj-indmced dopamine xelease in the accumbens in behaving aninals. Deehan and Roed, report on the rokt of salsonilpl anq other cmnjugates in acetaldwhyde self-adminisuration, in an integratibe revhew ov human findings and their own key animal data involving the mesolimbic dipaminxrdic system.

Amthoigh dmpcmiue has feen e major focus for studies of acetaldehyde's centrel actions, ocher neural systems are also onxolved. For inrtance, the role of the olioid syxtem in the neurochemical and brhavioral effects of acebaldehyde is rsviewed by Font and Pastor, wno not only discusw thc effects of sxlspnllol on mu opipd receptors, but also summarize whqt is jnlwn about acetalvehyde formabiun in brain nuclei rich in datamwse avd beta-endorpnine neurons. Ekegant studies condubteq by
those actions in different intracellular signaling systems brain A special on acetaldehyde formation, to reinforcing characteristics is by Diana and Emphasis is put on the use thiol compounds, which sequester acetaldehyde, as therapeutic agents preventing those effects. A very methodological approach using gene-specific manipulations to change enzymatic activity, both in the liver in brain, led and colleagues to explore the behavioral consequences of central versus peripheral acetaldehyde metabolism. Direct administration of or acetaldehyde either in the periphery or in brain, as employed in studies from Correa and Salamone's describe expression (a of activity) a broad range brain areas involved in the motivational actions of both compounds. At the molecular level, Weiger and colleagues data indicating acts on calcium-activated channels, key factor in of neural cells. The role of form tetrahydroisoquinoline alkaloids is presented in the next of articles. attention is paid to the conjugate acetaldehyde with dopamine, salsolinol. This molecule has demonstrated be central for the actions of ethanol in the mesolimbic system (Melis et al., 2013). presented by Xie, Ye colleagues show how modulates of neurons brain slices posterior ventral tegmental area via activation of opioid receptors located in GABAergic neurons. These data are discussed by Polache and Granero commentary, from the perspective their own extensive research salsonilol-induced release in the accumbens animals. and the of and other conjugates in self-administration, in an integrative review human findings and their the mesolimbic dopaminergic system. Although dopamine has been major focus for studies of acetaldehyde's central other neural systems are also involved. For instance, the role of the system in and behavioral effects of acetaldehyde is reviewed by and Pastor, who not discuss the effects of salsonilol on mu opiod receptors, also what is about acetaldehyde formation brain nuclei rich catalase and beta-endorphine studies conducted
 those actions in different inTracellulaR signAliNg sYsTems And dIverse brain areAS. A spEcial accent on acetaldehYde foRmATion, MEtAboliSm and blOCkADE in ReLaTioN tO ItS reinForCing chaRacteristiCs iS pResented by DiANa And colleagUes. emphasis is puT on The use Of ThiOL compOunDs, whiCh sequESter acEtaldehydE, aS TherapEUtic ageNTS pReveNting those effects. a VeRY interesting meThodolOgICaL APprOacH using gene-SpEcifiC ManipulATiONS To cHAnge enzymatic Activity, botH In tHe liveR aNd iN The braIn, has LeD isrAel and colleAgueS to explorE the beHAvioral COnsequeNces of CenTraL verSUs PeRipHeRAl aCEtAldEHydE metabolIsM. DIrect AdmiNISTRatiOn oF ethAnol oR acetaldehyde EitHer iN The PeripHery oR in tHe Brain, As emplOyed iN tHe studies from CoRrea And SalamoNe's LaB, deScRibe c-fOs exprEssIon (A marker Of neuraL ActIvITY) AcRoss a broad range of bRaIN ArEas involVed in tHE mOtIVational AcTioNs of BOTh comPounDS. AT the moleCular lEVeL, WEiger anD cOlleagUeS prEseNt datA IndiCating That acetAldehYDe acts on maxi caLCium-activated POtASSiUM chaNneLs, a key factoR in eLEctrIcal STiMulATion oF neurAl CElLS.

The role of acetaldehYdE/monoaMine cOnjugates that Form tetrahYDROisoquinOlinE AlKAloids is presenTed in The next groUP of articLes. SpEcial attEntion is pAID to the coNjuGatE of AceTALdEhyde with dopaMINe, saLsOlinol. THis MoleculE haS deMonStrAtEd to be cenTral for tHe AcTiOnS of EthanOL in the meSoLimBiC syStem (MELis et aL., 2013). ElecTropHySiOLogIcal datA PrESEnteD bY XIe, Ye And CoLleagUes sHOw hOw salsoLinol moduLatES firInG oF dopamiNe neurons in brAiN slices froM pOstErior vENTral tegmEntal area via activation oF Opioid rEcePtors LocaTed in neigHboRing GAbAeRGic neuRons. ThEse daTa Are DIScussED By polAcHe and GraneRO In a CommeNtAry, wRitten fRom the perspective oF TheIr own extensivE reSearCH On SalSOnILol-InDUceD DOpamine release iN the accumbEnS In Behaving anIMalS. DEehan anD Rodd, rePort oN The role Of salsoniLol and othEr ConjUGAteS in acetaldEhyde selF-administRAtion, IN aN inteGraTive reViEw oF humaN findiNGs aNd theIr own kEy Animal Data iNvOlving thE mesolimbic dopaminergic System.

althoUgh Dopamine hAs bEEn a Major focuS for Studies of aCetAldEhyde'S ceNTral aCtioNS, oTheR NeuraL sysTEms are alsO InVolVED. FOr instance, tHE ROle Of the OpiOId systEm in The neurochemical aND behavioral effEcts OF AceTalDEhydE iS reviewed by FonT anD PASTor, who noT oNly discuss tHe effectS oF SalsoNilol oN mu opiOd recepTORs, BUt also SummAriZe what is kNowN aBOut acetAlDeHYde forMatiOn In braiN nucleI Rich IN Catalase and beta-eNdorpHINe neuROns. elegaNt Studies COnduCted by
 those actions in differen t intracel lular  si gna li ng s yste ms and diverse brai n areas. A special acc ent o na ceta l de hydeformati o n, m eta bo li sman d  b locka dein rela tion to it s r ei nforcing cha r ac teristicsispresented by  Di ana an dcol l eague s.Empha sis is put on  the useof thiolc ompound s ,  w hich  sequester acetal d eh y de, as therape utic a ge n ts p rev ent ing thoseef fects .  A very in t e r est i ng methodolog ical approa c h u sing g en e-s p ecific  mani pu l ati ons to chan ge e nzymaticactivi t y, both in theliverand  in  the br ai n,ha s  le d  I sra e l a nd colle ag ue s toexpl o r e thebeh avio ral c onsequences o f c entr a l v ersus  peri pher al  acet aldehy de me ta bolism. Directadmi nistratio n o feth an ol or acetal deh yde  either  in the per ip h e r yor in the brain, a se m pl oyed inthe st u di es from Cor re a a nd S a l amone 's l a b,  describ e c-Fo s  e xp ression  ( a mark er  of  ne urala ctiv ity) a cross abroad range of brain areas involve d  i n th e  mot iva tional acti onso f bo th c o mp oun d s. At  themo l ec u lar level, Weiger a nd  colle agues  present data  indicatin g t hat acet alde h yd e  acts on maxicalci um-activat e d potass ium c hannels,  a key fa c t or in el ect ric alsti m u la tion of neura l cell s. 

The r ole  of ace tal deh yde /mo no amine con jugatesth at  f or m t etrah y droisoqu in oli ne  al kaloi d s is p resen tedin  t h e n ext gro u po f  art ic le s. S pec ia l att enti o n i s paidto the co nju g ateof  a cetalde hyde with dop am ine, salso li nol . This m oleculehas demonstrated to bec entralfor  theacti ons of et han ol inthe mesoli mbic s ystem  ( Mel i s  et a l . ,201 3) . Electrop h y sio logic al  dat a prese nted by Xie, Ye an d  co lleagues show  ho w sa l s ol ino l  m o dul at e s f i r ing of dopamine  neurons i nb ra in slicesf rom  p osterio r ventr al te g mentalarea viaactivatio nof o p i oid  receptors  located  in neigh b oring GA BAerg icneuron s.  Th ese d ata ar e  di scuss ed byPo lacheand G ra nero ina commentary, written f rom th e per spe ctive ofthe i r o wn extens iveresearch o n s als onilo l-i n duced  dop a mi ner eleas e in the accum b en s i n be having anim a l s . D eehan  an d  Rodd,  rep ort on the role o f  salsonilol an d ot h e r c onj u gate sin acetaldehyd e s el f - administ ra tion, in an  integra ti v e rev iew of  human  findin g s  a n d thei r ow n k ey animal  da ta involvi ng  t h e meso limb ic  dopam inergi c  sys t e m.

Although dop amine h as be e n a  majo rfocus f o r st udies of a cetaldehyde 's cen tral  acti ons, ot he r neur alsy stems area lso invol ved.For ins ta nce,  th e role  oft h e opi oidsy ste m in then e ur o ch em i cal  and  beha vi oral  effectso f acetal deh y de is r ev iew e d  by Fo n ta n d Pastor,who  noto n ly discuss thee ff e cts o f sals onilol  on muo pio drecepto rs, b ut also s ummarizew hat  i s kn own abou tacet al deh yd e formation inbrain nu clei ric h in cat ala s e an d  beta- en dorphine neu rons.  E l egant s t u die s condu c ted  by 
 those_actions in_different intracellular signaling systems_and diverse_brain_areas. A_special_accent on acetaldehyde_formation, metabolism and_blockade in relation to_its reinforcing characteristics_is_presented by Diana and colleagues. Emphasis is put on the use of thiol compounds,_which_sequester acetaldehyde,_as_therapeutic_agents preventing those effects. A_very interesting methodological approach using_gene-specific manipulations_to change enzymatic activity, both in the liver_and_in the brain,_has led Israel and colleagues to explore the behavioral_consequences of central versus peripheral acetaldehyde_metabolism. Direct administration_of_ethanol_or acetaldehyde either in_the periphery or in the brain,_as employed in the studies from_Correa and Salamone's lab, describe c-Fos expression_(a marker of neural activity) across_a broad range of brain_areas involved_in the motivational actions of_both compounds. At_the molecular_level, Weiger and_colleagues present data indicating that acetaldehyde_acts on maxi_calcium-activated potassium channels, a key factor_in_electrical stimulation of_neural_cells.

The_role of_acetaldehyde/monoamine conjugates that_form_tetrahydroisoquinoline alkaloids_is_presented in the next group of_articles._Special attention is paid to the conjugate_of acetaldehyde with dopamine,_salsolinol._This molecule has demonstrated_to be central for the_actions of ethanol in the mesolimbic_system (Melis_et al.,_2013). Electrophysiological data presented by Xie, Ye and colleagues show how_salsolinol modulates firing of dopamine neurons_in brain slices from_posterior ventral_tegmental_area via activation_of_opioid receptors_located in neighboring GABAergic neurons. These data_are discussed_by Polache and Granero in a_commentary, written from the_perspective_of their own extensive research on_salsonilol-induced dopamine release in the accumbens_in behaving animals. Deehan and_Rodd,_report_on the role of salsonilol_and other conjugates in acetaldehyde self-administration,_in an integrative_review of human findings and their own_key_animal data involving the mesolimbic dopaminergic_system.

Although_dopamine has been a major focus_for_studies_of acetaldehyde's central actions, other_neural systems are also involved. For_instance, the role of the opioid system in the_neurochemical and behavioral_effects of acetaldehyde is reviewed_by_Font_and Pastor, who not only discuss the effects of salsonilol_on mu_opiod receptors, but_also summarize what is known about acetaldehyde formation in brain_nuclei rich in catalase and beta-endorphine neurons._Elegant studies conducted by