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  • Muscarinic cholinergic receptor M1 in the rat basolateral amygdala: ultrastructural localization and synaptic relationships to cholinergic axons.

Muscarinic cholinergic receptor M1 in the rat basolateral amygdala: ultrastructural localization and synaptic relationships to cholinergic axons.

The Journal of comparative neurology (2013-04-06)
Jay F Muller, Franco Mascagni, Violeta Zaric, Alexander J McDonald
ABSTRACT

Muscarinic neurotransmission in the anterior basolateral amygdalar nucleus (BLa) mediated by the M1 receptor (M1R) is critical for memory consolidation. Although knowledge of the subcellular localization of M1R in the BLa would contribute to an understanding of cholinergic mechanisms involved in mnemonic function, there have been no ultrastructural studies of this receptor in the BLa. In the present investigation, immunocytochemistry at the electron microscopic level was used to determine which structures in the BLa express M1R. The innervation of these structures by cholinergic axons expressing the vesicular acetylcholine transporter (VAChT) was also studied. All perikarya of pyramidal neurons were labeled, and about 90% of dendritic shafts and 60% of dendritic spines were M1R+. Some dendrites had spines suggesting that they belonged to pyramidal cells, whereas others had morphological features typical of interneurons. M1R immunoreactivity (M1R-ir) was also seen in axon terminals, most of which formed asymmetrical synapses. The main targets of M1R+ terminals forming asymmetrical synapses were dendritic spines, most of which were M1R+. The main targets of M1R+ terminals forming symmetrical synapses were M1R+ perikarya and dendritic shafts. About three-quarters of VAChT+ cholinergic terminals formed synapses; the main postsynaptic targets were M1R+ dendritic shafts and spines. In some cases M1R-ir was seen near the postsynaptic membrane of these processes, but in other cases it was found outside of the active zone of VAChT+ synapses. These findings suggest that M1R mechanisms in the BLa are complex, involving postsynaptic effects as well as regulating release of neurotransmitters from presynaptic terminals.