Neuronal localization of m1 muscarinic receptor immunoreactivity in the rat basolateral amygdala.
Neuronal localization of m1 muscarinic receptor immunoreactivity in the rat basolateral amygdala.
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DOI：
10.1007/s00429-010-0272-y
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发表时间：
2010-07
影响因子：
3.1
通讯作者：
Mascagni F
中科院分区：
文献类型：
--
作者：
McDonald AJ;Mascagni F
杏仁核基底外侧核复合体（BLC）中的毒蕈碱胆碱能神经传递对情绪/动机学习任务中的记忆巩固至关重要。虽然在BLC的毒蕈碱受体亚型的本地化的知识将有助于理解的行动，乙酰胆碱在记忆功能，以前的受体结合和原位杂交研究缺乏必要的分辨率，以确定哪些神经元在BLC表达不同的受体亚型。在本研究中，免疫组织化学被用来研究神经元的M1受体的定位。M1免疫反应的强度在杏仁核的不同核团中各不相同，在BLC和相邻的后外侧皮质核中最强。BLC中标记神经元的密度和形态表明，M1+神经元群体包括锥体细胞，杏仁核区域的主要神经元。此外，在BLC的神经鞘中有密集的点状m1免疫反应。使用细胞类型特异性标记物的抗体进行BLC的双标记免疫荧光研究，以更明确地确定M1阳性（M1+）神经元的表型。钙/钙调蛋白蛋白激酶II（CaMK）的抗体用于标记锥体细胞，而谷氨酸脱羧酶的抗体用于标记中间神经元。几乎所有的强烈标记的M1+神经元的BLC的CaMK+锥体细胞。这些数据表明，M1受体拮抗剂损害BLC中记忆巩固的能力主要是由于阻断对锥体神经元活性的胆碱能影响。
Muscarinic cholinergic neurotransmission in the basolateral nuclear complex (BLC) of the amygdala is critical for memory consolidation in emotional/motivational learning tasks. Although knowledge of the localization of muscarinic receptor subtypes in the BLC would contribute to an understanding of the actions of acetylcholine in mnemonic function, previous receptor binding and in situ hybridization studies lacked the resolution necessary to identify which neurons in the BLC express different receptor subtypes. In the present study immunohistochemistry was used to study the neuronal localization of the m1 receptor. The intensity of m1 immunoreactivity varied in different nuclei of the amygdala, and was most robust in the BLC, and in the adjacent posterolateral cortical nucleus. The density and morphology of labeled neurons in the BLC suggested that the m1+ neuronal population included pyramidal cells, the principal neurons in this amygdalar region. In addition, there was dense punctate m1 immunoreactivity in the neuropil of the BLC. Dual labeling immunofluorescence studies of the BLC using antibodies to cell type specific markers were performed to more definitively determine the phenotype of m1-positive (m1+) neurons. An antibody to calcium/calmodulin protein kinase II (CaMK) was used to label pyramidal cells, whereas an antibody to glutamic acid decarboxylase was used to label interneurons. Virtually all of the intensely labeled m1+ neurons of the BLC were CaMK+ pyramidal cells. These data suggest that the ability of M1 receptor antagonists to impair memory consolidation in the BLC is mainly due to blockade of cholinergic influences on the activity of pyramidal neurons.