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Ethanol reduces excitability in a subgroup of primary sensory neurons by activation of BK Ca channels
Author(s) -
Gruß Marco,
Henrich Michael,
König Peter,
Hempelmann Gunter,
Vogel Werner,
Scholz Andreas
Publication year - 2001
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.0953-816x.2001.01754.x
Subject(s) - bk channel , chemistry , iberiotoxin , patch clamp , ethanol , neuron , nociception , voltage dependent calcium channel , biophysics , neuroscience , medicine , endocrinology , calcium , receptor , membrane potential , biochemistry , biology , organic chemistry
Ethanol effects on the central nervous system have been well investigated and described in recent years; modulations, by ethanol, of several ligand‐gated and voltage‐gated ion channels have been found. In this paper, we describe a shortening of action potential duration (APD) by ethanol in ≈ 40% of small diameter neurons in rat dorsal root ganglia (DRG). In these neurons, designated as group A neurons, we observed an ethanol‐induced increase in whole‐cell outward‐current. As iberiotoxin, a specific blocker of large‐conductance calcium‐activated K + channels (BK Ca channels), blocks the effects of ethanol, we investigated the interaction between these channels and ethanol in outside‐out patches. Open probability of BK Ca channels was increased 2–6 × depending on the concentration (40–80 m m ≈ 2–4‰ v/v) of ethanol. Functional consequences were a prolongation of the refractory period, which was reversible after addition of iberiotoxin, and reduced firing frequency during ethanol application. In contrast, another type of neuron (group B) showed a prolonged APD during application of ethanol which was irreversible in most cases. In 90% of cases, neurons of group A showed a positive staining for isolectin B4 (I‐B4), a marker for nociceptive neurons. We suggest that the activation of BK Ca channels induced by clinically relevant concentrations of ethanol, the resulting modulations of APD and refractory period of DRG neurons, might contribute to clinically well‐known ethanol‐induced analgesia and paresthesia.