期刊
NEURON
卷 33, 期 1, 页码 113-122出版社
CELL PRESS
DOI: 10.1016/S0896-6273(01)00557-8
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资金
- NIA NIH HHS [AG16678] Funding Source: Medline
- NIDA NIH HHS [DA09293, DA07304] Funding Source: Medline
- NIDCD NIH HHS [DC04200] Funding Source: Medline
- NIGMS NIH HHS [GM58710] Funding Source: Medline
Modulation of Ca2+, channels by neurotransmitters; provides critical control of neuronal excitability and synaptic strength. Little is known about regulation of the Ca2+ efflux pathways that counterbalance Call influx in neurons. We demonstrate that bradykinin and ATP significantly facilitate removal of action potential-induced Ca2+ loads by stimulating plasma membrane Ca2+-ATPases (PMCAs) in rat sensory neurons. This effect was mimicked in the soma and axonal varicosities by phorbol esters and was blocked by antagonists of protein kinase C (PKC). Reduced expression of PMCA isoform 4 abolished, and overexpression of isoform 4b enhanced, PKC-dependent facilitation of Ca2+ efflux. This acceleration of PMCA4 underlies the shortening of the action potential afterhyperpolarization produced by activation of bradykinin and purinergic receptors. Thus, isoform-specific modulation of PMCA-mediated Ca2+ efflux represents a novel mechanism to control excitability in sensory neurons.
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