GABA_A and GABA_B receptors have opposite effects on synaptic glutamate release on the nucleus tractus solitarii neurons

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• 作者：Y.-H. Kang^a ; B. Sun^a ; Y.S. Park^b ; C.-S. Park^b ; Y.-H. Jin^a ; ^{jinyh@khu.ac.kr}
• 关键词：GABA ; glutamate ; nucleus tractus solitarii (NTS) ; heterosynaptic modulation
• 刊名：Neuroscience
• 出版年：2012
• 期刊代码：50_03064522
• 类别：neu
• 出版时间：3 May, 2012
• 卷：209
• 期：Complete
• 页码：39-46
• 文件大小：1533 K

摘要

Cranial visceral afferent nerve transfers information about visceral organs to nucleus tractus solitarii (NTS) by releasing the excitatory neurotransmitter glutamate. Various endogenous modulators affect autonomic reflex responses by changing glutamatergic responses in the NTS. Although the expression of GABA_A and GABA_B receptors in glutamatergic terminals is known, their functional contribution on glutamate release is poorly characterized. Here, we used mechanically isolated NTS neurons to examine the mechanisms by which presynaptic GABA_A and GABA_B receptors modulate glutamatergic excitatory postsynaptic currents (EPSCs). EPSC were isolated by clamping voltage at equilibrium potential for chloride (鈭?9 mV) without any GABA receptors antagonists. In all neurons, GABA_A agonist, muscimol (1 and 10 渭M), increased EPSC frequency (284.1卤57%and 278.4卤87%of control, respectively), but the GABA_B agonist, baclofen (10 渭M), decreased EPSC frequency (43卤8%of control). The GABA_A antagonist, gabazine (18 渭M), decreased EPSC frequency in 50%of tested neurons, whereas GABA_B antagonist, CGP (5 渭M), increased the EPSC frequency in 36%of tested neurons. External application of GABA (1 and 30 渭M) facilitating the EPSC frequency. The facilitation of the GABA_A receptor-mediated release of glutamate was blocked by Na⁺-K⁺-Cl^{鈭?/sup> cotransporter type 1 antagonist or Na+ and Ca2+ channel inhibitors indicating GABA_A presynaptic depolarization. Thus, tonically released GABA activates GABA_A and GABA_B receptors to modulate the release of glutamate. These findings provide cellular mechanisms of heterosynaptic GABA-glutamate integration of peripheral visceral afferent signals in the NTS.}