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Voltage‐gated potassium channels of Schwann cells from trout lateral line nerve: A combined electrophysiological and molecular characterization
Author(s) -
Rabe H.,
Ritz H.J.,
Jeserich G.
Publication year - 1998
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/(sici)1098-1136(199808)23:4<329::aid-glia5>3.0.co;2-y
Subject(s) - biology , potassium channel , inward rectifier potassium ion channel , biophysics , electrophysiology , membrane potential , patch clamp , xenopus , excitatory postsynaptic potential , microbiology and biotechnology , ion channel , inhibitory postsynaptic potential , neuroscience , biochemistry , receptor , gene
Voltage‐gated ionic currents were recorded from explant cultured and freshly dissociated SC from trout lateral line nerve using the whole‐cell configuration of the patch clamp technique. In the majority of cases a delayed rectifier potassium outward current (K D ) was found exclusively, which activated at potentials ≥ −40 mV and reached maximal amplitudes of 240 ± 25.2 nA at 60 mV testpulse potential. This current showed no voltage‐dependent kinetics of inactivation and was insensitive to TEA but was effectively blocked by 4‐AP. By single cell RT‐PCR the transcript of a shaker‐related potassium channel gene, termed tsha1 (a fish homologue of Kv1.2), was selectively amplified. In its biophysical and pharmacological properties the native whole cell potassium outward current of trout Schwann cells closely matched those of the cloned tsha1 subunit previously expressed in xenopus oocytes. A small subpopulation of freshly dissociated SC (less than 10%) at hyperpolarizing potentials elicited a potassium inward current instead, which in its kinetics closely resembled the inward rectifier (K IR ) of mammalian SC. Neither voltage‐gated sodium currents nor membrane currents activated by excitatory amino acids (glutamate, kainate, and quisqualate) were observed. GLIA 23:329–338, 1998. © 1998 Wiley‐Liss, Inc.