Document Detail

Neuronal calcium sensor-1 facilitates neuronal exocytosis through phosphatidylinositol 4-kinase.
MedLine Citation:
PMID:  15659215     Owner:  NLM     Status:  MEDLINE    
This work tested the theory that neuronal calcium sensor-1 (NCS-1) has effects on neurotransmitter release beyond its actions on membrane channels. We used nerve-ending preparations where membrane channels are bypassed through membrane permeabilization made by mechanical disruption or streptolysin-O. Nerve ending NCS-1 and phosphatidylinositol 4-kinase (PI4K) are largely or entirely particulate, so their concentrations in nerve endings remain constant after breaching the membrane. Exogenous, myristoylated NCS-1 stimulated nerve ending phosphatidylinositol 4-phosphate [PI(4)P] synthesis, but non-myristoylated-NCS-1 did not. The N-terminal peptide of NCS-1 interfered with PI(4)P synthesis, and with spontaneous and Ca(2+)-evoked release of both [(3)H]-norepinephrine (NA) and [(14)C]-glutamate (glu) in a concentration-dependent manner. An antibody raised against the N-terminal of NCS-1 inhibited perforated nerve ending PI(4)P synthesis, but the C-terminal antibody had no effects. Antibodies against the N- and C-termini of NCS-1 caused significant increases in mini/spontaneous/stimulation-independent release of [(3)H]-NA from perforated nerve endings, but had no effect on [(14)C]-glu release. These results support the idea that NCS-1 facilitates nerve ending neurotransmitter release and phosphoinositide production via PI4K and localizes these effects to the N-terminal of NCS-1. Combined with previous work on the regulation of channels by NCS-1, the data are consistent with the hypothesis that a NCS-1-PI4K (NP, neuropotentiator) complex may serve as an essential linker between lipid and protein metabolism to regulate membrane traffic and co-ordinate it with ion fluxes and plasticity in the nerve ending.
Qian Zheng; Joseph A Bobich; Jolanta Vidugiriene; Susanne C McFadden; Fairwell Thomas; John Roder; Andreas Jeromin
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  92     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  2005 Feb 
Date Detail:
Created Date:  2005-01-20     Completed Date:  2005-06-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  England    
Other Details:
Languages:  eng     Pagination:  442-51     Citation Subset:  IM    
Department of Chemistry, Texas Christian University, Fort Worth, Texas, USA.
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MeSH Terms
1-Phosphatidylinositol 4-Kinase / chemistry,  drug effects,  metabolism*
Antibodies / pharmacology
Calcium / chemistry,  metabolism
Calcium-Binding Proteins / chemistry,  pharmacology,  physiology*
Cerebral Cortex / chemistry
Dose-Response Relationship, Drug
Exocytosis / drug effects,  physiology*
Nerve Endings / chemistry,  drug effects,  metabolism*
Nerve Tissue Proteins / chemistry,  pharmacology,  physiology*
Neuronal Calcium-Sensor Proteins
Neurons / chemistry*
Neurotransmitter Agents / chemistry,  metabolism
Peptide Fragments / pharmacology
Phosphatidylinositol 4,5-Diphosphate / biosynthesis,  chemistry
Phosphatidylinositol Phosphates / biosynthesis,  chemistry
Rats, Sprague-Dawley
Rats, Wistar
Subcellular Fractions / chemistry,  metabolism
Reg. No./Substance:
0/Antibodies; 0/Calcium-Binding Proteins; 0/Nerve Tissue Proteins; 0/Neuronal Calcium-Sensor Proteins; 0/Neuropeptides; 0/Neurotransmitter Agents; 0/Peptide Fragments; 0/Phosphatidylinositol 4,5-Diphosphate; 0/Phosphatidylinositol Phosphates; 0/frequenin calcium sensor proteins; 0/phosphatidylinositol 4-phosphate; 7440-70-2/Calcium; EC 4-Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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