| Literature DB >> 9535950 |
B Everill1, M A Rizzo, J D Kocsis.
Abstract
Outward K+ currents were recorded using a whole cell patch-clamp configuration, from acutely dissociated adult rat cutaneous afferent dorsal root ganglion (DRG) neurons (L4 and L5) identified by retrograde labeling with Fluoro-gold. Recordings were obtained 16-24 h after dissociation from cells between 39 and 49 mm in diameter with minimal processes. These cells represent medium-sized DRG neurons relative to the entire population, but are large cutaneous afferent neurons giving rise to myelinated axons. Voltage-activated K+ currents were recorded routinely during 300-ms depolarizing test pulses increasing in 10-mV steps from -40 to +50 mV; the currents were preceded by a 500-ms conditioning prepulse of either -120 or -40 mV. Coexpression of at least three components of K+ current was revealed. Separation of these components was achieved on the basis of sensitivities to the K+ channel blockers, 4-aminopyridine (4-AP) and dendrotoxin (DTx), and by the current responses to variation in conditioning voltage. Changing extracellular K+ concentration from 3 to 40 mM resulted in a shift to the right of the I-V curve commensurate with K+ being the principal charge carrier. Presentation of 100 mM 4-AP revealed a rapidly activating K+ current sensitive to low concentrations of 4-AP. High concentrations of 4-AP (6 mM) extinguished all inactivating current, leaving almost pure sustained current (IK). On the basis of the relative distribution of K+ currents neurons could be separated into three distinct categories: fast inactivating current (IA), slow inactivating current (ID), and sustained current (IK); only IA and IK; and slow inactivating current and IK. However, IK was always the dominant outward current component. These results indicate that considerable variation in K+ currents is present not only in the entire population of DRG neurons, as previously reported, but even within a restricted size and functional group (large cutaneous afferent neurons).Entities:
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Year: 1998 PMID: 9535950 PMCID: PMC2605378 DOI: 10.1152/jn.1998.79.4.1814
Source DB: PubMed Journal: J Neurophysiol ISSN: 0022-3077 Impact factor: 2.714