Elsevier

Neuroscience

Volume 25, Issue 3, June 1988, Pages 729-749
Neuroscience

Diversity and ubiquity of K channels

https://doi.org/10.1016/0306-4522(88)90033-4Get rights and content

Abstract

The following developments since this review was prepared and submitted (February, 1987) are important to the theme and conclusions made here: 1. Apamin block of Ca-activated K channels has now been observed in neurons of at least two mammalian brain areas: in neurosecretory neurons in the rat superoptic nucleus of the hypothalamus [Bourque C.W. and Brown D.A. (1987) Neurosci Lett.82, 185] and in neurons in the guinea-pig mammillary bodies (Alonso A., personal communication). In hippocampal neurons, a Ca-activated K channel which may be responsible for the slow AHP has been identified in single channel recordings. However, this channel has unique properties and it is not blocked by Apamin. This is another example that suggests that more than one subclass of Ca-activated K channel may mediate slow AHPs. Therefore, the term IAHP channel used in Table 5 for the Apamin-sensitive channel may be incorrect. 2. cDNAs for the “high threshold” “A” channel encoded in the Shaker gene locus in Drosophila have been cloned [Kamb A., Iverson L.E. and Tanouye M.A. (1987) Cell50, 405; Papazian D.M., Schwarz T.L., Tempel B.L., Jan Y.N. and Jan L.Y. (1987) Science237, 794]. The primary transcript of this gene undergoes extensive differential splicing generating a large diversity of products (Kamb A., Tseng-Crank J. and Tanouye M.A. Cell, submitted). At least three of these express “A” currents in Xenopus oocytes (Iverson L.E., Davidson N., Lester H., Tanouye M. and Rudy B. Proc. Natn. Acad. Sci., U.S.A., submitted; Timpe L.C., Schwarz T.L., Tempel B.L., Papazian D.M. Jan Y.N. and Jan L.Y. Nature, in press), which differ in inactivation kinetics. In all cases, however, the voltage-dependence of activation and inactivation is similar among the various clones and distinct from the “low threshold” “A” channels (Table 3). It is possible then that the Shaker “A” channel is a subclass of “A” channels (see Table 4) that then diversifies into distinct types. Knowledge of the molecular relationship between the Shaker “A” channels, the “low-threshold” “A” channels (Table 3) and other voltage-dependent K channels may eventually help in establishing a hierarchy of K channel diversification into classes, subclasses and types as suggested here. 3. G protein subunits may also activate K channels directly in the CNS [Andrade R., Malenka R.A. and Nicoll R.A. (1986) Science234, 1261]. 4. A book on ion-channel modulation, with many examples of modulation of K channels was published: Kaczmareck L.K. and Levitan I.B. (1987) Neuromodulation: The Biochemical Control of Neuronal Excitability. Oxford University Press, New York.

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