Cromwell H C, Levine M S
Mental Retardation Research Center, University of California at Los Angeles 90024, USA.
Neuroscience. 1996 Nov;75(2):361-72. doi: 10.1016/0306-4522(96)00315-6.
The present experiments were designed to investigate the physiological impact of a partial decortication upon neostriatal synaptic responses using intracellular recording techniques in the in vitro brain slice preparation. In the intact rat, the locally evoked neostriatal synaptic response is primarily mediated by excitatory amino acid receptor activation. Following neocortex damage, the contributions of both N-methyl-D-aspartate and non-N-methyl-D-aspartate receptor activation were significantly diminished, although responses remained robust in amplitude and duration. Components of the locally evoked synaptic response mediated by activation of GABAA receptors were relatively unchanged, while presynaptic inhibition mediated by activation of GABAB receptors was markedly reduced. Furthermore, the normally minimal acetylcholine contribution to the synaptic response was significantly increased after neocortical damage. This enhanced cholinergic role in the generation of the synaptic response appeared to be mediated primarily by activation of nicotinic receptors. Thus, neocortical damage leads to novel physiological relationships between intrinsic neostriatal cholinergic interneurons and the GABAergic projection neurons. One possibility is that cholinergic interneurons have the potential for substituting for the loss of excitation created by the absence of neocortical glutamatergic input.
本实验旨在利用体外脑片制备中的细胞内记录技术，研究部分去皮质对新纹状体突触反应的生理影响。在完整的大鼠中，局部诱发的新纹状体突触反应主要由兴奋性氨基酸受体激活介导。新皮质损伤后，N-甲基-D-天冬氨酸和非N-甲基-D-天冬氨酸受体激活的贡献均显著降低，尽管反应在幅度和持续时间上仍然很强。由GABAA受体激活介导的局部诱发突触反应成分相对未变，而由GABAB受体激活介导的突触前抑制则明显减弱。此外，新皮质损伤后，通常对突触反应贡献极小的乙酰胆碱显著增加。这种胆碱能在突触反应产生中的增强作用似乎主要由烟碱受体激活介导。因此，新皮质损伤导致新纹状体内源性胆碱能中间神经元与GABA能投射神经元之间出现新的生理关系。一种可能性是，胆碱能中间神经元有可能替代因新皮质谷氨酸能输入缺失而产生的兴奋丧失。
