量子幅度的差异反映了两类丘脑神经元上皮质丘脑突触处GluR4亚基的数量。
Differences in quantal amplitude reflect GluR4- subunit number at corticothalamic synapses on two populations of thalamic neurons.
作者信息
Golshani P, Liu X B, Jones E G
机构信息
Center for Neuroscience, University of California, Davis, CA 95616, USA.
出版信息
Proc Natl Acad Sci U S A. 2001 Mar 27;98(7):4172-7. doi: 10.1073/pnas.061013698. Epub 2001 Feb 27.
Abstract
Low-frequency thalamocortical oscillations that underlie drowsiness and slow-wave sleep depend on rhythmic inhibition of relay cells by neurons in the reticular nucleus (RTN) under the influence of corticothalamic fibers that branch to innervate RTN neurons and relay neurons. To generate oscillations, input to RTN predictably should be stronger so disynaptic inhibition of relay cells overcomes direct corticothalamic excitation. Amplitudes of excitatory postsynaptic conductances (EPSCs) evoked in RTN neurons by minimal stimulation of corticothalamic fibers were 2.4 times larger than in relay neurons, and quantal size of RTN EPSCs was 2.6 times greater. GluR4-receptor subunits labeled at corticothalamic synapses on RTN neurons outnumbered those on relay cells by 3.7 times, providing a basis for differences in synaptic strength.
摘要
构成嗜睡和慢波睡眠基础的低频丘脑皮质振荡取决于网状核（RTN）中的神经元对中继细胞的节律性抑制，这一过程受皮质丘脑纤维的影响，这些纤维分支并支配RTN神经元和中继神经元。为了产生振荡，RTN的输入应该更强，这样中继细胞的双突触抑制就能克服皮质丘脑的直接兴奋。通过对皮质丘脑纤维进行最小刺激在RTN神经元中诱发的兴奋性突触后电导（EPSC）幅度比中继神经元中的大2.4倍，并且RTN的EPSC量子大小大2.6倍。RTN神经元上皮质丘脑突触处标记的GluR4受体亚基数量比中继细胞上的多3.7倍，这为突触强度的差异提供了基础。
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