Ethanol reduces excitability in a subgroup of primary sensory neurons by activation of BKCa channels

Marco Gruß, Michael Henrich, Peter König, Gunter Hempelmann, Werner Vogel, Andreas Scholz*

*Korrespondierende/r Autor/-in für diese Arbeit
51 Zitate (Scopus)


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 (BKCa channels), blocks the effects of ethanol, we investigated the interaction between these channels and ethanol in outside-out patches. Open probability of BKCa channels was increased 2-6 × depending on the concentration (40-80 mM ≈ 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 BKCa 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.

ZeitschriftEuropean Journal of Neuroscience
Seiten (von - bis)1246-1256
PublikationsstatusVeröffentlicht - 2001


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