Attenuation of Stimulated Accumbal Dopamine Release by NMDA Is Mediated through Metabotropic Glutamate Receptors

被引:1
作者
Spencer, Felicity S. E. [1 ]
Glodkowska, Maria [1 ]
Sebold, Anna I. [1 ]
Yavas, Ersin [2 ]
Young, Andrew M. J. [1 ]
机构
[1] Univ Leicester, Sch Psychol & Vis Sci, Leicester LE1 9HN, England
[2] Bartin Univ, Dept Psychol, TR-74100 Bartin, Turkiye
来源
ACS CHEMICAL NEUROSCIENCE | 2023年 / 14卷 / 08期
基金
英国生物技术与生命科学研究理事会;
关键词
Brain slices; dopamine; fast-scan cyclic voltammetry; metabotropic glutamate receptors; N-methyl-D-aspartate (NMDA); nucleus accumbens; SUBUNIT MESSENGER-RNAS; NUCLEUS-ACCUMBENS; CHOLINERGIC INTERNEURONS; MODULATE DOPAMINE; SCHIZOPHRENIA; TRANSMISSION; PHENCYCLIDINE; ANTAGONIST; KETAMINE; RAT;
D O I
10.1021/acschemneuro.2c00777
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Electrically stimulated dopamine release from the nucleus accumbens is attenuated following application of N-methyl-D-aspartate (NMDA), which is likely to be mediated indirectly through intermediary neuronal mechanisms rather than by a direct action on dopamine terminals. On the basis of known modulatory processes in nucleus accumbens, the current experiments sought to test whether the effect of NMDA was mediated through cholinergic, GABA-ergic, or metabotropic glutamatergic intermediate mechanisms. Fast-scan cyclic voltammetry was used to measure electrically stimulated dopamine release in nucleus accumbens of rat brain slices in vitro. Stimulated dopamine release was attenuated by NMDA, confirming previous findings, but this attenuation was unaffected by either cholinergic or GABA-ergic antagonists. However, it was completely abolished by the nonselective group I/II/III metabotropic glutamate receptor antagonist alpha-methyl-4-carboxyphenylglycine (MCPG) and by the selective group II antagonist LY 341396. Therefore, group II metabotropic glutamate receptors, but not acetylcholine or GABA receptors, mediate the attenuation of stimulated dopamine release caused by NMDA, probably by presynaptic inhibition through receptors located extra-synaptically on dopamine terminals. This provides a plausible mechanism for the documented role of metabotropic glutamate receptor systems in restoring deficits induced by NMDA receptor antagonists, modeling schizophrenia, underlining the potential for drugs affecting these receptors as therapeutic agents in treating schizophrenia.
引用
收藏
页码:1449 / 1458
页数:10
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