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200 nm in young rats (3–5 month old Fisher 344 rats) which remains normal in old (25–30 month rats) cerebral myocytes. Consistent with a healthy MaxiK channel expression in old cerebral arteries, MaxiK current density, kinetics and Ca2+ sensitivity were practically identical in young and old myocytes. Sensitivity to nanomolar concentrations of dehydrosoyasaponin-I that activates channels formed by α and β subunits is also the same in young and old myocytes. These results demonstrate that MaxiK channels maintain normal expression during cerebral aging which is in sharp contrast to our previous finding of loss of expression in aging coronary arteries. It seems therefore, that cerebral myocytes have developed a protective anti-aging mechanism leading to the continued expression of MaxiK channels.
doi:10.1016/0014-5793(96)00151-2 
Copyright © 1996 Published by Elsevier Science B.V.
Research letter
A calcium switch for the functional coupling between α (hslo) and β subunits (KV, Caβ) of maxi K channels
P. Meera, M. Wallner, Z. Jiang and L. Toro
, 
Dept. of Anesthesiology, BH-612 CHS Box 951778, University of California, Los Angeles, CA 90095-1778, USA
Received 11 January 1996.
| Referred to by: | | Corrigendum to: A calcium switch for the functional coupling between α (hslo) and β subunits (KV, Caβ) of maxi K channels FEBS Letters, Volume 385, Issues 1-2, 29 April 1996, Pages 127-128  PDF (87 K)
|
Abstract
KV,Caβ subunit dramatically increases the apparent calcium sensitivity of the α subunit of MaxlK channels when probed in the micromolar [Ca2+]i range. Analysis in a wide range of [Ca2+]i revealed that this functional coupling is exquisitely modulated by [Ca2+]i. Ca2+ ions switch MaxiK α+β complex into a functionally coupled state at concentrations beyond resting [Ca2+]i. At [Ca2+] ≤ 100 nM, MaxiK activity becomes independent of Ca2+, is purely voltage-activated, and its functional coupling with its β subunit is released. The functional switch develops at [Ca2+]i that occur during cellular excitation, providing the molecular basis of how MaxiK channels regulate smooth muscle excitability and neurotransmitter release.
Author Keywords: MaxiK channel; Calcium-independent activation; Calcium-dependent activation; Human myometrium; Subunit interaction α-β
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