Lavine N, Reuben M, Clarke P B
Department of Pharmacology and Therapeutics, McGill University, Montréal, Québec, Canada.
J Comp Neurol. 1997 Apr 7;380(2):175-90. doi: 10.1002/(sici)1096-9861(19970407)380:2<175::aid-cne3>3.0.co;2-0.
In the adult rat brain, a prominent population of nicotinic cholinoceptors binds 3H-nicotine with nanomolar affinity. These receptors are abundant in most thalamic nuclei and in neocortical layers 3/4, which receive a major thalamic input. To test whether cortical nicotinic receptors are associated with thalamocortical afferents, unilateral excitotoxic (N-methyl-D-aspartate) lesions were made in one of four thalamic nuclear groups (anterior, ventral, medial geniculate, or dorsal lateral geniculate) or in temporal cortex. After 1 or 4 weeks of survival, cortical 3H-nicotine binding was quantified via autoradiography. Thalamic lesions resulted in a partial loss of 3H-nicotine binding in ipsilateral cerebral cortex. In each thalamic lesion group, the greatest decrease (35-45%) occurred within the cortical layers and area (i.e., cingulate, parietal, temporal, or occipital cortex) receiving the densest thalamocortical innervation. Binding of 3H-nicotine was also reduced within the thalamus local to the lesion, particularly at the longer survival time. Saturation analysis, performed in frontoparietal cortical tissue homogenates following ventral thalamic lesions, revealed a significant (34%) reduction in receptor density but not affinity. Direct excitotoxic lesions of the neocortex (temporal cortex) tended to preserve 3H-nicotine binding in layers 3/4, despite local neuronal loss. These results, taken with other published findings, suggest that some nicotinic cholinoceptors in adult rat cerebral cortex are located on thalamocortical terminals. This organizing principle appears to apply not only to sensory and motor relay projections but also to association nuclei that project to allocortical areas. These receptors may provide a local mechanism for nicotinic cholinergic modulation of thalamocortical input.
在成年大鼠脑中,大量烟碱型胆碱能受体以纳摩尔亲和力结合³H-尼古丁。这些受体在大多数丘脑核团以及接受主要丘脑输入的新皮质第3/4层中大量存在。为了测试皮质烟碱型受体是否与丘脑皮质传入纤维相关,在四个丘脑核团(前核、腹核、内侧膝状体或背外侧膝状体)之一或颞叶皮质中进行了单侧兴奋性毒性(N-甲基-D-天冬氨酸)损伤。存活1周或4周后,通过放射自显影对皮质³H-尼古丁结合进行定量分析。丘脑损伤导致同侧大脑皮质³H-尼古丁结合部分丧失。在每个丘脑损伤组中,最大降幅(35%-45%)出现在接受最密集丘脑皮质神经支配的皮质层和区域(即扣带回、顶叶、颞叶或枕叶皮质)。损伤局部的丘脑内³H-尼古丁结合也减少,尤其是在较长存活时间时。对丘脑腹侧损伤后的额顶叶皮质组织匀浆进行饱和分析,结果显示受体密度显著降低(34%),但亲和力未降低。新皮质(颞叶皮质)的直接兴奋性毒性损伤尽管局部神经元丧失,但倾向于保留第3/4层中的³H-尼古丁结合。这些结果与其他已发表的研究结果表明,成年大鼠大脑皮质中的一些烟碱型胆碱能受体位于丘脑皮质终末。这种组织原则似乎不仅适用于感觉和运动中继投射,也适用于投射到异皮质区域的联合核团。这些受体可能为烟碱能对丘脑皮质输入的胆碱能调节提供一种局部机制。