Premium
Long‐Term Modulation of A‐Type K + Conductances in Hippocampal CA 1 Interneurons in Rats After Chronic Intermittent Ethanol Exposure During Adolescence or Adulthood
Author(s) -
Li Qiang,
Fleming Rebekah L.,
Acheson Shawn K.,
Madison Roger D.,
Moore Scott D.,
Risher MaryLouise,
Wilson Wilkie A.,
Swartzwelder H. Scott
Publication year - 2013
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/acer.12204
Subject(s) - hippocampal formation , ethanol , hippocampus , neuroscience , modulation (music) , term (time) , chemistry , medicine , endocrinology , physics , psychology , biochemistry , quantum mechanics , acoustics
Background Chronic alcohol use, especially exposure to alcohol during adolescence or young adulthood, is closely associated with cognitive deficits that may persist into adulthood. Therefore, it is essential to identify possible neuronal mechanisms underlying the observed deficits in learning and memory. Hippocampal interneurons play a pivotal role in regulating hippocampus‐dependent learning and memory by exerting strong inhibition on excitatory pyramidal cells. The function of these interneurons is regulated not only by synaptic inputs from other types of neurons but is also precisely governed by their own intrinsic membrane ionic conductances. The voltage‐gated A‐type potassium current ( I A ) regulates the intrinsic membrane properties of neurons, and disruption of I A is responsible for many neuropathological processes including learning and memory deficits. Thus, it represents a previously unexplored cellular mechanism whereby chronic ethanol ( E t OH ) may alter hippocampal memory‐related functioning. Methods Using whole‐cell electrophysiological recording methods, we investigated the enduring effects of chronic intermittent ethanol (CIE) exposure during adolescence or adulthood on I A in rat CA 1 interneurons. Results We found that the mean peak amplitude of I A was significantly reduced after CIE in either adolescence or adulthood, but I A density was attenuated after CIE in adolescence but not after CIE in adulthood. In addition, the voltage‐dependent steady‐state activation and inactivation of I A were altered in interneurons after CIE . Conclusions These findings suggest that CIE can cause long‐term changes in I A channels in interneurons and thus may alter their inhibitory influences on memory‐related local hippocampal circuits, which could be, in turn, responsible for learning and memory impairments observed after chronic E t OH exposure.