Abstract：
:Initial clearance of extracellular K+ ([K+]o) following neuronal excitation occurs by astrocytic uptake, because elevated [K+]o activates astrocytic but not neuronal Na+,K+-ATPases. Subsequently, astrocytic K+ is re-released via Kir4.1 channels after distribution in the astrocytic functional syncytium via gap junctions. The dispersal ensures widespread release, preventing renewed [K+]o increase and allowing neuronal Na+,K+-ATPase-mediated re-uptake. Na+,K+-ATPase operation creates extracellular hypertonicity and cell shrinkage which is reversed by the astrocytic cotransporter NKCC1. Inhibition of Kir channels by activation of specific PKC isotypes may decrease syncytial distribution and enable physiologically occurring [K+]o increases to open L-channels for Ca2+, activating [K+]o-stimulated gliotransmitter release and regulating gap junctions. Learning is impaired when [K+]o is decreased to levels mainly affecting astrocytic membrane potential or Na+,K+-ATPase or by abnormalities in its α2 subunit. It is enhanced by NKCC1-mediated ion and water uptake during the undershoot, reversing neuronal inactivity, but impaired in migraine with aura in which [K+]o is highly increased. Vasopressin augments NKCC1 effects and facilitates learning. Enhanced myelination, facilitated by astrocytic-oligodendrocytic gap junctions also promotes learning.
journal_name
Neurosci Biobehav Revjournal_title
Neuroscience and biobehavioral reviewsauthors
Hertz L,Chen Ydoi
10.1016/j.neubiorev.2016.09.018subject
Has Abstractpub_date
2016-12-01 00:00:00pages
484-505eissn
0149-7634issn
1873-7528pii
S0149-7634(16)30252-4journal_volume
71pub_type
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