Title

Membrane Microdomains And Neural Impulse Propagation: Field Effects In Cytoskeleton Corrals

Abstract

The possibility that an ensemble of neural-membrane lipids could regulate the duration of the ion-channel "open" conformation may have direct implications for local gating of the action potential (AP). The control of channel dynamics is equivalent to controlling the transmembrane ion conductances responsible for neural depolarization and hyperpolarization. Accordingly, if a membrane region in an axon were to contain (for example) clusters of Na+ channels with relatively longer open states, such a structure would be conducive to a local depolarization (spike) and the continuing propagation of the neural impulse. By contrast, if the Na+ channels had brief open states, the structure would be conducive to impulse propagation failure. Modulation of the membrane state through other channel types would of course also be possible. A good example is the A-current delayed-rectifier K+ channel (KA), currently the object of intensive research because of its possible role in conduction failure. The KA channel is gated by membrane hyperpolarization, which it increases and prolongs by rapidly conducting potassium ions out of the cytosol. A prolonged open time for this channel could hypothetically strengthen the delayed-rectifier effect and significantly increase the probability of conduction block. This chapter examines the possible role of neural membrane microdomains in regulating the propagation of the action potential. These data are particularly important because they appear consistent with the concept that "local switches" regulate AP propagation (Scott, 1995). The chapter begins with an overview of the experimental evidence for AP conduction failure. It then examines the two major alternative models: one emphasizing the role of impedance mismatch due to neuron branching geometry; the other emphasizing the role of prolonged hyperpolarization due to the A-current potassium channel (KA). A model emphasizing the possible interaction of a microdomain-cytoskeleton system with neuron branching geometry will then be presented (Wallace, 2004). Because of the large number of studies bearing on the subject, the KA channel will be used as the basic example, although the possible contributions of other channel types will be briefly discussed. The chapter concludes with a discussion of how microdomain regulation of AP propagation may explain a number of neuron features that strikingly depart from cable properties. © 2010 by Nova Science Publishers, Inc. All rights reserved.

Publication Date

12-1-2010

Publication Title

Cytoskeleton: Cell Movement, Cytokinesis and Organelles Organization

Number of Pages

161-176

Document Type

Article; Book Chapter

Personal Identifier

scopus

Socpus ID

84892799810 (Scopus)

Source API URL

https://api.elsevier.com/content/abstract/scopus_id/84892799810

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