期刊
MOLECULAR NEUROBIOLOGY
卷 38, 期 2, 页码 153-166出版社
SPRINGER
DOI: 10.1007/s12035-008-8039-7
关键词
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
资金
- National Science Foundation [0619427]
- National Institute Health [GM083049]
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM083049] Funding Source: NIH RePORTER
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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