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Role in neuronal cell migration for high‐threshold potassium currents in the chicken hindbrain
Author(s) -
Hendriks Richard,
Morest D. Kent,
Kaczmarek Leonard K.
Publication year - 1999
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19991215)58:6<805::aid-jnr7>3.0.co;2-v
Subject(s) - potassium channel , tetraethylammonium chloride , potassium , potassium channel blocker , chemistry , tetraethylammonium , patch clamp , biophysics , 4 aminopyridine , calcium , medicine , endocrinology , neuroscience , biochemistry , biology , receptor , organic chemistry
We have investigated the influence of voltage‐dependent, potassium conductances on the migration of embryonic neurons, using a culture preparation taken from the acoustico‐vestibular anlage long before the onset of electrical excitability and synaptic function. Whole‐cell patch clamp recordings from migrating neuroblasts at Hamburger‐Hamilton stage 28 (E 5.5) revealed the exclusive expression of voltage‐dependent, high‐threshold, outward currents, activating at potentials positive to ‐20 mV. These currents were completely suppressed by the potassium channel blockers, 1.0 mM tetraethylammonium chloride (TEA) or 1.0 mM 4‐aminopyridine (4‐AP). In control media, the active migration of individual neuroblasts was recorded at 27 ± 6 μm per hr. Within minutes after adding either drug to the culture, normal migration completely stopped for several hours. Calcium channel blockers, ω‐conotoxin (3 μM) or cadmium chloride (100 μM), slowed, but did not halt, migration, while nickel chloride (100 μM) or N‐methyl‐D‐glucamine (1 mM) had no effect. However, within 8 hr after TEA exposure, migratory activity usually returned. This recovery was associated with the appearance of a previously undetected, low‐threshold and 4‐AP‐ sensitive potassium conductance. We suggest that high‐threshold, TEA/4‐AP‐sensitive potassium channels may normally support the migration of these neurons, while their chronic blockade can be compensated by the appearance of novel potassium channels. Potassium currents may act in concert with N‐type calcium channels to regulate neuronal migration. J. Neurosci. Res. 58:805–814, 1999. © 1999 Wiley‐Liss, Inc.