Literature DB >> 34525325

On the electrical passivity of astrocyte potassium conductance.

Min Zhou1, Yixing Du1, Sydney Aten1, David Terman2.   

Abstract

Predominant expression of leak-type K+ channels provides astrocytes a high membrane permeability to K+ ions and a hyperpolarized membrane potential that are crucial for astrocyte function in brain homeostasis. In functionally mature astrocytes, the expression of leak K+ channels creates a unique membrane K+ conductance that lacks voltage-dependent rectification. Accordingly, the conductance is named ohmic or passive K+ conductance. Several inwardly rectifying and two-pore domain K+ channels have been investigated for their contributions to passive conductance. Meanwhile, gap junctional coupling has been postulated to underlie the passive behavior of membrane conductance. It is now clear that the intrinsic properties of K+ channels and gap junctional coupling can each act alone or together to bring about a passive behavior of astrocyte conductance. Additionally, while the passive conductance can generally be viewed as a K+ conductance, the actual representation of this conductance is a combined expression of multiple known and unknown K+ channels, which has been further modified by the intricate morphology of individual astrocytes and syncytial gap junctional coupling. The expression of the inwardly rectifying K+ channels explains the inward-going component of passive conductance disobeying Goldman-Hodgkin-Katz constant field outward rectification. However, the K+ channels encoding the outward-going passive currents remain to be determined in the future. Here, we review our current understanding of ion channels and biophysical mechanisms engaged in the passive astrocyte K+ conductance, propose new studies to resolve this long-standing puzzle in astrocyte physiology, and discuss the functional implication(s) of passive behavior of K+ conductance on astrocyte physiology.

Entities:  

Keywords:  astrocytes; gap junctions; patch-clamp; potassium channels

Mesh:

Substances:

Year:  2021        PMID: 34525325      PMCID: PMC8560416          DOI: 10.1152/jn.00330.2021

Source DB:  PubMed          Journal:  J Neurophysiol        ISSN: 0022-3077            Impact factor:   2.974


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