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J Neurophysiol. 2009 Mar;101(3):1494-506. doi: 10.1152/jn.91149.2008. Epub 2009 Jan 21.

Distinct subtypes of cholecystokinin (CCK)-containing interneurons of the basolateral amygdala identified using a CCK promoter-specific lentivirus.

Author information

1
Department of Psychiatry and Behavioral Sciences, Center for Behavioral Neuroscience, Yerkes Research Center, Emory University School of Medicine, Atlanta, Georgia, USA. ajasnow@emory.edu

Abstract

The basolateral amygdala (BLA) is critical for the formation of emotional memories. Little is known about the physiological properties of BLA interneurons, which can be divided into four subtypes based on their immunocytochemical profiles. Cholecystokinin (CCK) interneurons play critical roles in feedforward inhibition and behavioral fear responses. Evidence suggests that interneurons within a subgroup can display heterogeneous physiological properties. However, little is known about the physiological properties of CCK interneurons in the BLA and/or whether they represent a homogeneous or heterogeneous population. To address this question, we generated a lentivirus-expressing GFP under the control of the CCK promoter to identify CCK neurons in vivo. We combined this with whole cell patch-clamp recording techniques to examine the physiological properties of CCK-containing interneurons of the rat BLA. Here, we describe the physiological properties of 57 cells recorded in current-clamp mode; we used hierarchical cluster and discriminant function analysis to demonstrate that CCK interneurons can be segregated into three distinct subtypes (I, II, III) based on their passive and active membrane properties. Additionally, Type II neurons could be further separated into adapting and nonadapting types based on their rates of spike frequency adaptation. These data suggest that CCK interneurons of the BLA are a heterogeneous population and may be functionally distinct subpopulations that differentially contribute to the processing of emotionally salient stimuli.

PMID:
19164102
PMCID:
PMC2666417
DOI:
10.1152/jn.91149.2008
[Indexed for MEDLINE]
Free PMC Article

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