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首页> 外文期刊>Progress in brain research >GABAergic inhibition in the neostriatum.
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GABAergic inhibition in the neostriatum.

机译：新纹状体中的GABA能抑制。

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In the neostriatum, GABAergic inhibition arises from the action of at least two classes of inhibitory interneurons, and from recurrent collaterals of the principal cells. Interneurons receive excitatory input only from extrinsic sources, and so act in a purely feedforward capacity. Feedback inhibition arises from the recurrent collaterals of the principal cells. These two kinds of inhibition have functionally distinct effects on the principal cells. Inputs from interneurons are not very convergent. There are few inhibitory neurons, and so each principal cell receives inhibitory synaptic input from very few interneurons. But, they are individually powerful, and a single interneuron can substantially delay action potentials in a group of nearby principal cells. Recurrent inhibition is highly convergent, with each principal cell receiving inhibitory input from several hundred other such cells. Feedback inhibitory synaptic inputs individually have very weak effects, as seen from the soma. The differences in synaptic strength are not caused by differences in the release of transmitter or in sensitivity of the postsynaptic membrane. Rather, they arise from differences in the number of synaptic contacts formed on individual principal cells by feedforward or feedback axons, and from differences in synaptic location. Interneurons form their powerful synapses near the somata of principal cells, while most feedback synapses are more distal, where they interact with the two-state nonlinear properties of the principal cells' dendrite. This arrangement suggests that feedforward inhibition may serve in the traditional role for inhibition, adjusting the excitability of the principle neuron near the site of action potential generation. Feedback inhibitory synapses may interact with voltage-sensitive conductances in the dendrite to alter the electrotonic structure of the spiny cell.
机译：在新纹状体中，GABA能抑制起因于至少两类抑制性中间神经元的作用以及主要细胞的反复侧支。中间神经元仅从外部来源获得兴奋性输入，因此仅以前馈的方式起作用。反馈抑制源自原代细胞的反复侧支。这两种抑制作用对原代细胞具有功能上不同的作用。来自中间神经元的输入不是很收敛。抑制神经元很少，因此每个主要细胞都从很少的中间神经元接收抑制性突触输入。但是，它们具有强大的功能，单个中间神经元可以大大延迟附近一组主要细胞中的动作电位。复发抑制高度收敛，每个主要细胞都从数百个其他此类细胞接收抑制输入。从躯体中可以看出，反馈抑制性突触输入的作用非常弱。突触强度的差异不是由递质释放或突触后膜敏感性的差异引起的。相反，它们是由前馈或反馈轴突在单个主细胞上形成的突触接触数量的差异以及突触位置的差异引起的。内部神经元在主细胞的躯体附近形成强大的突触，而大多数反馈突触则在远端，与主要细胞的树突的两个状态的非线性特性相互作用。这种安排表明，前馈抑制作用可能起传统的抑制作用，从而调节了主神经元在动作电位产生部位附近的兴奋性。反馈抑制突触可能与树突中的电压敏感电导相互作用，以改变棘突细胞的电渗结构。

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