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Cell‐type‐specific tonic GABA signaling in the rat central amygdala is selectively altered by acute and chronic ethanol
Author(s) -
Herman Melissa Ann,
Roberto Marisa
Publication year - 2016
Publication title -
addiction biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.445
H-Index - 78
eISSN - 1369-1600
pISSN - 1355-6215
DOI - 10.1111/adb.12181
Subject(s) - tonic (physiology) , inhibitory postsynaptic potential , receptor , chemistry , neuroscience , population , bursting , gabaa receptor , endocrinology , medicine , biology , biochemistry , environmental health
The central nucleus of the amygdala ( CeA ) is an important site for the reinforcing effects of ethanol and has been implicated in the development of alcohol dependence. The CeA GABA A receptor system is particularly vulnerable to the effects of acute and chronic ethanol exposure. Previous work in the CeA focused on ethanol and phasic GABA A receptor signaling, but tonic GABA A receptor signaling in the rat CeA remains understudied. In the present study, we found that the CeA contains two types of tonic conductance that are expressed in a cell‐type‐specific manner. Low threshold bursting ( LTB ) and some regular spiking ( RS ) neurons have an ongoing tonic conductance that is mediated by the α1‐ GABA A receptor subunit and is insensitive to acute ethanol exposure. Late spiking ( LS ) and a separate population of RS neurons do not display a persistent tonic conductance but have the potential for tonic signaling that is mediated by the δ‐ GABA A receptor subunit and can be activated by increasing the ambient GABA concentration or by acute ethanol exposure. Acute ethanol exposure differentially alters the firing discharge of different CeA cell types. Chronic ethanol exposure produces a switch in tonic signaling such that the tonic conductance in LTB and some RS neurons is lost and an ongoing tonic conductance is present in LS and a separate population of RS neurons. Collectively, these data demonstrate cell‐type‐specific tonic signaling in the CeA and provide new insight into how acute and chronic ethanol exposure differentially alter specific aspects of inhibitory circuitry in the CeA .