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首页> 外文期刊>The European Journal of Neuroscience >Nigral GABAergic inhibition upon mesencephalic dopaminergic cell groups in rats.
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Nigral GABAergic inhibition upon mesencephalic dopaminergic cell groups in rats.

机译：黑色素GABA能对大鼠中脑多巴胺能细胞群的抑制作用。

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Abstract Synaptic inhibition from the substantia nigra pars reticulata (SNr) to the mesencephalic dopaminergic neurons, which was mediated by gamma (gamma)-amino-butyric acid (GABA), was investigated in a midbrain slice preparation of Wistar rats. Whole-cell patch-clamp recordings were used to record synaptic potentials/currents from the dopaminergic neurons (n = 93) located in the retrorubral field (n = 22), the substantia nigra pars compacta (n = 47) and the ventral tegmental area (n = 24). In the presence of ionotropic glutamate receptor antagonists electrical stimulation of the SNr induced inhibitory postsynaptic potentials (IPSPs) and/or currents (IPSCs) in 83 neurons. The IPSPs/IPSCs were comprised early and late components. The early IPSPs/IPSCs were mediated by chloride currents through GABA(A) receptors. The late IPSPs/IPSCs were mediated by potassium currents through GABA(B) receptors. Both GABA(A)- and GABA(B)-IPSPs were amplified by repetitive stimuli with frequencies between 25 and 200 Hz.This frequency range covers the firing frequencies of SNr neurons in vivo. It was observed that an application of a GABA(B) receptor antagonist increased the amplitude of the GABA(A)-IPSPs. The amplification was followed by a rebound depolarization that induced transient firing of dopaminergic neurons. These properties of the IPSPs were common in all of the three dopaminergic nuclei. These results suggest that postsynaptic GABA(A)- and GABA(B)-inhibition contribute to transient and persistent alternations of the excitability of dopaminergic neurons, respectively. These postsynaptic mechanisms may be, in turn, regulated by presynaptic GABA(B)-inhibition. Nigral GABAergic input may provide the temporospatial regulation of the background excitability of mesencephalic dopaminergic systems.
机译：摘要在Wistar大鼠的中脑切片制备中，研究了γ-氨基丁酸（GABA）介导的网状黑质（SNr）对中脑多巴胺能神经元的突触抑制作用。使用全细胞膜片钳记录来记录位于后房区（n = 22），黑质致密部（n = 47）和腹侧被盖区的多巴胺能神经元（n = 93）的突触电位/电流。 （n = 24）。在离子型谷氨酸受体拮抗剂的存在下，SNr的电刺激在83个神经元中诱导了抑制性突触后电位（IPSP）和/或电流（IPSC）。 IPSP / IPSC由早期和晚期组成。早期的IPSP / IPSC是通过GABA（A）受体的氯离子电流介导的。晚期IPSPs / IPSCs通过GABA（B）受体的钾电流介导。 GABA（A）-和GABA（B）-IPSPs均通过重复刺激以25至200 Hz的频率进行扩增，该频率范围涵盖了体内SNr神经元的激发频率。观察到，使用GABA（B）受体拮抗剂会增加GABA（A）-IPSP的幅度。扩增后是反弹多极化，引起多巴胺能神经元的瞬时放电。 IPSP的这些特性在所有三个多巴胺能核中都很常见。这些结果表明，突触后GABA（A）和GABA（B）抑制分别促成多巴胺能神经元兴奋性的瞬时和持续交替。这些突触后机制又可以通过突触前GABA（B）抑制来调节。黑色素GABA能量输入可提供中脑多巴胺能系统背景兴奋性的颞pat调节。

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