Role in neuronal cell migration for high-threshold potassium currents in the chicken hindbrain

We have investigated the influence of voltage-dependent, potassium conducta nces on the migration of embryonic neurons, using a culture preparation tak en 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 complete ly suppressed by the potassium channel blockers, 1.0 mM tetraethylammonium chloride (TEA) or 1.0 mM 4-aminopyridine (4-AP), In control media, the acti ve migration of individual neuroblasts was recorded at 27 +/- 6 mu m per hr , Within minutes after adding either drug to the culture, normal migration completely stopped for several hours. Calcium channel blockers, co-conotoxi n (3 mu M) or cadmium chloride (100 mu M), slowed, but did not halt, migrat ion, while nickel chloride (100 mu M) or N-methyl-D-glucamine (1 mM) had no effect. However, within 8 hr after TEA exposure, migratory activity usuall y returned. This recovery was associated with the appearance of a previousl y undetected, low-threshold and 4-AP- sensitive potassium conductance. We s uggest that high-threshold, TEA/4-AP-sensitive potassium channels may norma lly support the migration of these neurons, while their chronic blockade ca n be compensated by the appearance of novel potassium channels. Potassium c urrents may act in concert with N-type calcium channels to regulate neurona l migration, J. Neurosci, Res. 58:805-814, 1999, (C) 1999 Wiley-Liss, Inc.