Journal
MOLECULAR NEUROBIOLOGY
Volume 38, Issue 2, Pages 153-166Publisher
SPRINGER
DOI: 10.1007/s12035-008-8039-7
Keywords
Calcium/calmodulin-dependent protein kinase II (CaMKII); Neurotransmitter release; BK channel; Slo; Slo1; SLO-1; Maxi-K channel; Synapsin; Ca(V)2.1; Calcium channel; Ryanodine receptor; Synaptotagmin; SNARE
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Funding
- National Science Foundation [0619427]
- National Institute Health [GM083049]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM083049] Funding Source: NIH RePORTER
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Ca2+/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 Ca2+ 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 neuro transmitter 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.
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