Bradykinin and ATP Accelerate Ca2+ Efflux from Rat Sensory Neurons via Protein Kinase C and the Plasma Membrane Ca2+ Pump Isoform 4

Yuriy M Usachev; Steven J DeMarco; Colin Campbell; Emanuel E Strehler; Stanley A Thayer

doi:10.1016/S0896-6273(01)00557-8

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Bradykinin and ATP Accelerate Ca2+ Efflux from Rat Sensory Neurons via Protein Kinase C and the Plasma Membrane Ca2+ Pump Isoform 4

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Bradykinin and ATP Accelerate Ca2+ Efflux from Rat Sensory Neurons via Protein Kinase C and the Plasma Membrane Ca2+ Pump Isoform 4

Yuriy M Usachev, Steven J DeMarco, Colin Campbell, Emanuel E Strehler and Stanley A Thayer

Neuron (Cambridge, Mass.), Vol.33(1), pp.113-122

01/2002

DOI: 10.1016/S0896-6273(01)00557-8

PMID: 11779484

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Abstract

Modulation of Ca(2+) channels by neurotransmitters provides critical control of neuronal excitability and synaptic strength. Little is known about regulation of the Ca(2+) efflux pathways that counterbalance Ca(2+) influx in neurons. We demonstrate that bradykinin and ATP significantly facilitate removal of action potential-induced Ca(2+) loads by stimulating plasma membrane Ca(2+)-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 Ca(2+) 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 Ca(2+) efflux represents a novel mechanism to control excitability in sensory neurons.

Details

Title: Subtitle: Bradykinin and ATP Accelerate Ca2+ Efflux from Rat Sensory Neurons via Protein Kinase C and the Plasma Membrane Ca2+ Pump Isoform 4
Creators: Yuriy M Usachev
Steven J DeMarco
Colin Campbell
Emanuel E Strehler
Stanley A Thayer
Resource Type: Journal article
Publication Details: Neuron (Cambridge, Mass.), Vol.33(1), pp.113-122
DOI: 10.1016/S0896-6273(01)00557-8
PMID: 11779484
ISSN: 0896-6273
eISSN: 1097-4199
Grant note: DOI: 10.13039/100000001, name: National Science Foundation, award: IBN0110409; DOI: 10.13039/100000002, name: National Institutes of Health, award: AG16678, DA07304, DA09293, DC04200, GM58710
Language: English
Date published: 01/2002
Academic Unit: Iowa Neuroscience Institute; Anesthesia; Neuroscience and Pharmacology
Record Identifier: 9984040470502771

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