Neuronal localization of m1 muscarinic receptor immunoreactivity in the rat basolateral amygdala.

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.