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Neuron. 1995 Oct;15(4):951-60.

Modulation of K+ current by frequency and external [K+]: a tale of two inactivation mechanisms.

Author information

1
Department of Neurobiology, Harvard Medical School, Massachusetts General Hospital, Boston 02114, USA.

Abstract

Voltage-activated K+ currents and their inactivation properties are important for controlling frequency-dependent signaling in neurons and other excitable cells. Two distinct molecular mechanisms for K+ channel inactivation have been described: N-type, which involves rapid occlusion of the open channel by an intracellular tethered blocker, and C-type, which involves a slower change at the extracellular mouth of the pore. We find that frequency-dependent cumulative inactivation of Shaker channels is very sensitive to changes of extracellular [K+] in the physiological range, with much more inactivation at low [K+]out, and that it results from the interaction of N- and C-type inactivation. N-type inactivation enhances C-type inactivation by two mechanisms. First, it inhibits outward K+ flux, which normally fills an external ion site and thus prevents C-type inactivation. Second, it keeps the channel's activation gate open even after repolarization, allowing C-type inactivation to occur for a prolonged period.

PMID:
7576643
DOI:
10.1016/0896-6273(95)90185-x
[Indexed for MEDLINE]
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