Functional somato-dendritic alpha7-containing nicotinic acetylcholine receptors in the rat basolateral amygdala complex.

Published

Journal Article

Multiple subtypes of nicotinic acetylcholine receptors (nAChRs) are expressed in the CNS. The amygdala complex, the limbic structure important for emotional memory formation, receives cholinergic innervation from the basal forebrain. Although cholinergic drugs have been shown to regulate passive avoidance performance via the amygdala, the neuronal subtypes and circuits involved in this regulation are unknown. In the present study, whole-cell patch-clamp electrophysiological techniques were used to identify and characterize the presence of functional somato-dendritic nAChRs within the basolateral complex of the amygdala. Pressure-application of acetylcholine (ACh; 2 mm) evoked inward current responses in a subset of neurons from both the lateral (49%) and basolateral nuclei (72%). All responses displayed rapid activation kinetics, and were blocked by the alpha7-selective antagonist methyllycaconitine. In addition, the alpha7-selective agonist choline induced inward current responses that were similar to ACh-evoked responses. Spiking patterns were consistent with pyramidal class I neurons (the major neuronal type in the basolateral complex); however, there was no correlation between firing frequency and the response to ACh. The local photolysis of caged carbachol demonstrated that the functional expression of nAChRs is located both on the soma and dendrites. This is the first report demonstrating the presence of functional nAChR-mediated current responses from rat amygdala slices, where they may be playing a significant role in fear and aversively motivated memory.

Full Text

Duke Authors

Cited Authors

  • Klein, RC; Yakel, JL

Published Date

  • November 1, 2006

Published In

Volume / Issue

  • 576 / Pt 3

Start / End Page

  • 865 - 872

PubMed ID

  • 16931547

Pubmed Central ID

  • 16931547

International Standard Serial Number (ISSN)

  • 0022-3751

Digital Object Identifier (DOI)

  • 10.1113/jphysiol.2006.118232

Language

  • eng

Conference Location

  • England