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 Neurobioljournal_title
Molecular neurobiologyauthors
Wang ZWdoi
10.1007/s12035-008-8039-7subject
Has Abstractpub_date
2008-10-01 00:00:00pages
153-66issue
2eissn
0893-7648issn
1559-1182journal_volume
38pub_type
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