Compounds > 6-(1h-imidazol-1-yl)-7-nitro-2-3(1h-4h)-quinoxalinedione

6-(1h-imidazol-1-yl)-7-nitro-2-3(1h-4h)-quinoxalinedione and alpha-methyl-4-carboxyphenylglycine

6-(1h-imidazol-1-yl)-7-nitro-2-3(1h-4h)-quinoxalinedione has been researched along with alpha-methyl-4-carboxyphenylglycine* in 1 studies

Other Studies

1 other study(ies) available for 6-(1h-imidazol-1-yl)-7-nitro-2-3(1h-4h)-quinoxalinedione and alpha-methyl-4-carboxyphenylglycine

Article	Year
Group II metabotropic glutamate receptors are a common target of N-anisoyl-GABA and 1S,3R-ACPD in enhancing ACh release in the prefrontal cortex of freely moving SHRSP. Neuropharmacology, 2000, Mar-03, Volume: 39, Issue:5 Aniracetam is a therapeutically useful cognition enhancer for treating various neuropsychiatric symptoms occurring after cerebral infarction. We recently reported that local perfusion of its major metabolites N-anisoyl-GABA and p-anisic acid, but not aniracetam itself, enhanced acetylcholine (ACh) release with a delayed onset in cerebral regions of stroke-prone spontaneously hypertensive rats (SHRSP). In this study, we examined the possible involvement of metabotropic and ionotropic glutamate (mGlu and AMPA) receptors in the N-anisoyl-GABA-induced ACh release using brain in vivo microdialysis. Basal ACh release in SHRSP was commonly lower in the nucleus reticularis thalami, dorsal hippocampus and prefrontal cortex than that in age-matched Wistar Kyoto rats. The delayed ACh release in the prefrontal cortex of SHRSP was completely blocked by MCPG, a group I and II mGlu receptor antagonist, and MCCG, a group II-selective mGlu receptor antagonist. In contrast, it was largely unaffected by AIDA, a group I-selective mGlu receptor antagonist, or by YM90K, an AMPA receptor antagonist. 1S,3R-ACPD, a preferential group II mGlu receptor agonist, enhanced ACh release with a similar latency and the effect was antagonized by MCCG, whereas AMPA induced a prompt ACh release. These results indicate that N-anisoyl-GABA and 1S,3R-ACPD share a common mechanism mediated by group II mGlu receptors in enhancing ACh release. The findings suggest a possible mechanism for aniracetam's clinical efficacy in stroke patients with cholinergic deficits. Topics: Acetylcholine; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amino Acids, Dicarboxylic; Animals; Anisoles; Benzoates; Cycloleucine; Dose-Response Relationship, Drug; Excitatory Amino Acid Antagonists; Glycine; Hippocampus; Indans; Male; Microdialysis; Perfusion; Prefrontal Cortex; Quinoxalines; Rats; Rats, Inbred SHR; Receptors, AMPA; Receptors, Metabotropic Glutamate; Thalamic Nuclei; Wakefulness	2000

Article

Year

Group II metabotropic glutamate receptors are a common target of N-anisoyl-GABA and 1S,3R-ACPD in enhancing ACh release in the prefrontal cortex of freely moving SHRSP.

Neuropharmacology, 2000, Mar-03, Volume: 39, Issue:5

Aniracetam is a therapeutically useful cognition enhancer for treating various neuropsychiatric symptoms occurring after cerebral infarction. We recently reported that local perfusion of its major metabolites N-anisoyl-GABA and p-anisic acid, but not aniracetam itself, enhanced acetylcholine (ACh) release with a delayed onset in cerebral regions of stroke-prone spontaneously hypertensive rats (SHRSP). In this study, we examined the possible involvement of metabotropic and ionotropic glutamate (mGlu and AMPA) receptors in the N-anisoyl-GABA-induced ACh release using brain in vivo microdialysis. Basal ACh release in SHRSP was commonly lower in the nucleus reticularis thalami, dorsal hippocampus and prefrontal cortex than that in age-matched Wistar Kyoto rats. The delayed ACh release in the prefrontal cortex of SHRSP was completely blocked by MCPG, a group I and II mGlu receptor antagonist, and MCCG, a group II-selective mGlu receptor antagonist. In contrast, it was largely unaffected by AIDA, a group I-selective mGlu receptor antagonist, or by YM90K, an AMPA receptor antagonist. 1S,3R-ACPD, a preferential group II mGlu receptor agonist, enhanced ACh release with a similar latency and the effect was antagonized by MCCG, whereas AMPA induced a prompt ACh release. These results indicate that N-anisoyl-GABA and 1S,3R-ACPD share a common mechanism mediated by group II mGlu receptors in enhancing ACh release. The findings suggest a possible mechanism for aniracetam's clinical efficacy in stroke patients with cholinergic deficits.

Topics: Acetylcholine; alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid; Amino Acids, Dicarboxylic; Animals; Anisoles; Benzoates; Cycloleucine; Dose-Response Relationship, Drug; Excitatory Amino Acid Antagonists; Glycine; Hippocampus; Indans; Male; Microdialysis; Perfusion; Prefrontal Cortex; Quinoxalines; Rats; Rats, Inbred SHR; Receptors, AMPA; Receptors, Metabotropic Glutamate; Thalamic Nuclei; Wakefulness

2000