Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices
T. Opitz, P. Richter, A. J. Carter, A. P. Kozikowski, H. Shinozaki, K. G. Reymann
Hippocampal slices were transiently exposed to an oxygen- and glucose-free environment which causes a pronounced drop of both ATP and creatine phosphate, an anoxic depolarization, and an incomplete recovery of synaptically evoked population spike in the CA1 region after 1 h (48.5 ± 3.6% of baseline values). This recovery could be markedly enhanced by the application of N-methyl-d-aspartate receptor antagonists. To examine the influence of metabotropic glutamate receptors on neuronal recovery from hypoxia/ hypoglycemia, we applied various antagonists and agonists of the metabotropic glutamate receptors to the bath during the interval from 20 min before to 10 min after hypoxia/hypoglycemia. The metabotropic glutamate receptor antagonists (+)-α-methyl-4-carboxyphenylglycine and l-2-amino-3-phosphonopropionic acid were both able to enhance the population spike recovery significantly. However, the mixed metabotropic glutamate receptor agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid also exhibited a protective effect on population spike recovery, leaving the anoxic depolarization and N-methyl-d-aspartate responses during the hypoxia/hypoglycemia untouched. With the help of more subtype-specific agonists, we found that an activation of phospholipase C coupled (class 1) metabotropic glutamate receptors prior to hypoxia/hypoglycemia may be responsible for the protective effect seen with 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid, because the specific class 1 metabotropic glutamate receptor agonist trans-azetidine-2,4-dicarboxylic acid appeared to be highly protective, but only if it was applied 20 min before the hypoxia/hypoglycemia. An activation of class 2 metabotropic glutamate receptors by (2S1′R,2′R,3′R)-2-(2,3-dicarboxycycloprophyl)glycine, which inhibits adenylyl cyclase activity, led to a marked deterioration of the population spike recovery and even to a total prevention of the protective effect of the N-methyl-d-aspartate agonist d-2-amino-5-phosphonopentanoic acid. Our data suggest that prior activation of class 1 metabotropic glutamate receptors is beneficial, while their activation during hypoxia/hypoglycemia is detrimental. Furthermore, the activation of class 2 metabotropic glutamate receptors decreases the recovery from hypoxia/hypoglycemia.
https://doi.org/10.1016/0306-4522(95)00195-O
10.1016/0306-4522(95)00195-O
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Metabotropic Glutamate Receptors Medicine & Life Sciences 100%
Hypoglycemia Medicine & Life Sciences 77%
Hypoxia Medicine & Life Sciences 62%
1-amino-1,3-dicarboxycyclopentane Medicine & Life Sciences 36%
metabotropic glutamate receptor 2 Medicine & Life Sciences 35%
In Vitro Techniques Medicine & Life Sciences 34%
metabotropic glutamate receptor type 1 Medicine & Life Sciences 32%
Excitatory Amino Acid Agonists Medicine & Life Sciences 31%
Opitz, T., Richter, P., Carter, A. J., Kozikowski, A. P., Shinozaki, H., & Reymann, K. G. (1995). Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices. Neuroscience, 68(4), 989-1001. https://doi.org/10.1016/0306-4522(95)00195-O
Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices. / Opitz, T.; Richter, P.; Carter, A. J.; Kozikowski, A. P.; Shinozaki, H.; Reymann, K. G.
In: Neuroscience, Vol. 68, No. 4, 10.1995, p. 989-1001.
Opitz, T, Richter, P, Carter, AJ, Kozikowski, AP, Shinozaki, H & Reymann, KG 1995, 'Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices', Neuroscience, vol. 68, no. 4, pp. 989-1001. https://doi.org/10.1016/0306-4522(95)00195-O
Opitz T, Richter P, Carter AJ, Kozikowski AP, Shinozaki H, Reymann KG. Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices. Neuroscience. 1995 Oct;68(4):989-1001. https://doi.org/10.1016/0306-4522(95)00195-O
Opitz, T. ; Richter, P. ; Carter, A. J. ; Kozikowski, A. P. ; Shinozaki, H. ; Reymann, K. G. / Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices. In: Neuroscience. 1995 ; Vol. 68, No. 4. pp. 989-1001.
@article{c7990da3a2fe4f41ad796756456631bf,
title = "Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices",
abstract = "Hippocampal slices were transiently exposed to an oxygen- and glucose-free environment which causes a pronounced drop of both ATP and creatine phosphate, an anoxic depolarization, and an incomplete recovery of synaptically evoked population spike in the CA1 region after 1 h (48.5 ± 3.6% of baseline values). This recovery could be markedly enhanced by the application of N-methyl-d-aspartate receptor antagonists. To examine the influence of metabotropic glutamate receptors on neuronal recovery from hypoxia/ hypoglycemia, we applied various antagonists and agonists of the metabotropic glutamate receptors to the bath during the interval from 20 min before to 10 min after hypoxia/hypoglycemia. The metabotropic glutamate receptor antagonists (+)-α-methyl-4-carboxyphenylglycine and l-2-amino-3-phosphonopropionic acid were both able to enhance the population spike recovery significantly. However, the mixed metabotropic glutamate receptor agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid also exhibited a protective effect on population spike recovery, leaving the anoxic depolarization and N-methyl-d-aspartate responses during the hypoxia/hypoglycemia untouched. With the help of more subtype-specific agonists, we found that an activation of phospholipase C coupled (class 1) metabotropic glutamate receptors prior to hypoxia/hypoglycemia may be responsible for the protective effect seen with 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid, because the specific class 1 metabotropic glutamate receptor agonist trans-azetidine-2,4-dicarboxylic acid appeared to be highly protective, but only if it was applied 20 min before the hypoxia/hypoglycemia. An activation of class 2 metabotropic glutamate receptors by (2S1′R,2′R,3′R)-2-(2,3-dicarboxycycloprophyl)glycine, which inhibits adenylyl cyclase activity, led to a marked deterioration of the population spike recovery and even to a total prevention of the protective effect of the N-methyl-d-aspartate agonist d-2-amino-5-phosphonopentanoic acid. Our data suggest that prior activation of class 1 metabotropic glutamate receptors is beneficial, while their activation during hypoxia/hypoglycemia is detrimental. Furthermore, the activation of class 2 metabotropic glutamate receptors decreases the recovery from hypoxia/hypoglycemia.",
author = "T. Opitz and P. Richter and Carter, {A. J.} and Kozikowski, {A. P.} and H. Shinozaki and Reymann, {K. G.}",
note = "Funding Information: Acknowledgements--The authors wish to thank Rosi Ewen, Sabine Hartmann, Ute Miiller, Jeannette Witzke and Elke Wohlfarth for expert technical assistance. We also thank Drs Nikolai B. Fedorov and Thomas Behnisch for helpful advice in micropressure and intracellular recordings. This research was supported in part by grants of the German Ministry for Science and Technology (BEO 21-0319998A and BEO 21-0319520B) and the Biomed I program (BMH1-CT93-1033).",
doi = "10.1016/0306-4522(95)00195-O",
pages = "989--1001",
journal = "Neuroscience",
T1 - Metabotropic glutamate receptor subtypes differentially influence neuronal recovery from in vitro hypoxia/hypoglycemia in rat hippocampal slices
AU - Opitz, T.
AU - Richter, P.
AU - Carter, A. J.
AU - Kozikowski, A. P.
AU - Shinozaki, H.
AU - Reymann, K. G.
N1 - Funding Information: Acknowledgements--The authors wish to thank Rosi Ewen, Sabine Hartmann, Ute Miiller, Jeannette Witzke and Elke Wohlfarth for expert technical assistance. We also thank Drs Nikolai B. Fedorov and Thomas Behnisch for helpful advice in micropressure and intracellular recordings. This research was supported in part by grants of the German Ministry for Science and Technology (BEO 21-0319998A and BEO 21-0319520B) and the Biomed I program (BMH1-CT93-1033).
N2 - Hippocampal slices were transiently exposed to an oxygen- and glucose-free environment which causes a pronounced drop of both ATP and creatine phosphate, an anoxic depolarization, and an incomplete recovery of synaptically evoked population spike in the CA1 region after 1 h (48.5 ± 3.6% of baseline values). This recovery could be markedly enhanced by the application of N-methyl-d-aspartate receptor antagonists. To examine the influence of metabotropic glutamate receptors on neuronal recovery from hypoxia/ hypoglycemia, we applied various antagonists and agonists of the metabotropic glutamate receptors to the bath during the interval from 20 min before to 10 min after hypoxia/hypoglycemia. The metabotropic glutamate receptor antagonists (+)-α-methyl-4-carboxyphenylglycine and l-2-amino-3-phosphonopropionic acid were both able to enhance the population spike recovery significantly. However, the mixed metabotropic glutamate receptor agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid also exhibited a protective effect on population spike recovery, leaving the anoxic depolarization and N-methyl-d-aspartate responses during the hypoxia/hypoglycemia untouched. With the help of more subtype-specific agonists, we found that an activation of phospholipase C coupled (class 1) metabotropic glutamate receptors prior to hypoxia/hypoglycemia may be responsible for the protective effect seen with 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid, because the specific class 1 metabotropic glutamate receptor agonist trans-azetidine-2,4-dicarboxylic acid appeared to be highly protective, but only if it was applied 20 min before the hypoxia/hypoglycemia. An activation of class 2 metabotropic glutamate receptors by (2S1′R,2′R,3′R)-2-(2,3-dicarboxycycloprophyl)glycine, which inhibits adenylyl cyclase activity, led to a marked deterioration of the population spike recovery and even to a total prevention of the protective effect of the N-methyl-d-aspartate agonist d-2-amino-5-phosphonopentanoic acid. Our data suggest that prior activation of class 1 metabotropic glutamate receptors is beneficial, while their activation during hypoxia/hypoglycemia is detrimental. Furthermore, the activation of class 2 metabotropic glutamate receptors decreases the recovery from hypoxia/hypoglycemia.
AB - Hippocampal slices were transiently exposed to an oxygen- and glucose-free environment which causes a pronounced drop of both ATP and creatine phosphate, an anoxic depolarization, and an incomplete recovery of synaptically evoked population spike in the CA1 region after 1 h (48.5 ± 3.6% of baseline values). This recovery could be markedly enhanced by the application of N-methyl-d-aspartate receptor antagonists. To examine the influence of metabotropic glutamate receptors on neuronal recovery from hypoxia/ hypoglycemia, we applied various antagonists and agonists of the metabotropic glutamate receptors to the bath during the interval from 20 min before to 10 min after hypoxia/hypoglycemia. The metabotropic glutamate receptor antagonists (+)-α-methyl-4-carboxyphenylglycine and l-2-amino-3-phosphonopropionic acid were both able to enhance the population spike recovery significantly. However, the mixed metabotropic glutamate receptor agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid also exhibited a protective effect on population spike recovery, leaving the anoxic depolarization and N-methyl-d-aspartate responses during the hypoxia/hypoglycemia untouched. With the help of more subtype-specific agonists, we found that an activation of phospholipase C coupled (class 1) metabotropic glutamate receptors prior to hypoxia/hypoglycemia may be responsible for the protective effect seen with 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid, because the specific class 1 metabotropic glutamate receptor agonist trans-azetidine-2,4-dicarboxylic acid appeared to be highly protective, but only if it was applied 20 min before the hypoxia/hypoglycemia. An activation of class 2 metabotropic glutamate receptors by (2S1′R,2′R,3′R)-2-(2,3-dicarboxycycloprophyl)glycine, which inhibits adenylyl cyclase activity, led to a marked deterioration of the population spike recovery and even to a total prevention of the protective effect of the N-methyl-d-aspartate agonist d-2-amino-5-phosphonopentanoic acid. Our data suggest that prior activation of class 1 metabotropic glutamate receptors is beneficial, while their activation during hypoxia/hypoglycemia is detrimental. Furthermore, the activation of class 2 metabotropic glutamate receptors decreases the recovery from hypoxia/hypoglycemia.
U2 - 10.1016/0306-4522(95)00195-O
DO - 10.1016/0306-4522(95)00195-O
JO - Neuroscience
JF - Neuroscience