Regulation of synaptic transmission by presynaptic CaMKII and BK channels.

Abstract:

:Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) and the BK channel are enriched at the presynaptic nerve terminal, where CaMKII associates with synaptic vesicles whereas the BK channel colocalizes with voltage-sensitive Ca(2+) channels in the plasma membrane. Mounting evidence suggests that these two proteins play important roles in controlling neurotransmitter release. Presynaptic BK channels primarily serve as a negative regulator of neurotransmitter release. In contrast, presynaptic CaMKII either enhances or inhibits neurotransmitter release and synaptic plasticity depending on experimental or physiological conditions and properties of specific synapses. The different functions of presynaptic CaMKII appear to be mediated by distinct downstream proteins, including the BK channel.

journal_name

Mol Neurobiol

journal_title

Molecular neurobiology

authors

Wang ZW

doi

10.1007/s12035-008-8039-7

subject

Has Abstract

pub_date

2008-10-01 00:00:00

pages

153-66

issue

2

eissn

0893-7648

issn

1559-1182

journal_volume

38

pub_type

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