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Do Glial Gap Junctions Play a Role in Extracellular Ion Homeostasis?

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Gap Junctions in the Nervous System

Part of the book series: Neuroscience Intelligence Unit ((NIU.LANDES))

Abstract

In the adult mammalian brain, glial cells, to a much greater extent than neurons, express the intriguing form of intercellular communication that is mediated by gap junctions1,2 (see also chapters 8, 11). The function(s) served by glial gap junctions is not clearly established. One long held notion is that electrical coupling between glial cells, mediated by these junctions, helps to redistribute K+ that accumulates with neural activity, the so-called spatial buffer hypothesis3 (see below). Although there is strong evidence that K+ release associated with intense neural activity would quickly overwhelm diffusion-based K+ removal leading to disruptive increases in extracellular [K+] ([K+]0),4–6 there is no evidence-based consensus about how the brain prevents this from happening. This fact is not widely appreciated. The theories about [K+]0 homeostasis, especially spatial buffering, have been around for so long that they are sometimes mistakenly assumed to be proven. I will briefly review what is known about control of brain [K+]0 and discuss possible roles of glial gap junctions in these processes.

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Ransom, B.R. (1996). Do Glial Gap Junctions Play a Role in Extracellular Ion Homeostasis?. In: Gap Junctions in the Nervous System. Neuroscience Intelligence Unit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-21935-5_9

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  • DOI: https://doi.org/10.1007/978-3-662-21935-5_9

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