Document Detail


Modulation of a voltage-gated calcium channel linked to activation of glutamate receptors and calcium-induced calcium release in the catfish retina.
MedLine Citation:
PMID:  11507157     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. Catfish (Ictalurus punctatus) retinal cone horizontal cells contain an L-type calcium current that has been proposed to be involved in visual processing. Here we report on the modulation of this current by activation of glutamate receptors and calcium-induced calcium release (CICR) from intracellular calcium stores. 2. Fluorescence data obtained from isolated horizontal cells loaded with indo-1 provided evidence of calcium release from an intracellular calcium store sensitive to caffeine, calcium and ryanodine. In the presence of caffeine, ryanodine-sensitive stores released calcium in a transient manner. Release of calcium was blocked when cells were preincubated in BAPTA, in the presence of ruthenium red, or in low concentrations of ryanodine. 3. The release of calcium from ryanodine-sensitive stores directly corresponded with a decrease of the voltage-gated L-type calcium current amplitude. Caffeine-induced modulation of the calcium current was reduced in the presence of ruthenium red. 4. Activation of ionotropic kainate receptors on catfish cone horizontal cells triggered CICR from ryanodine-sensitive stores and mimicked inhibition of the voltage-gated calcium current. Kainate-induced inhibition of the calcium current was diminished when intracellular calcium stores were inhibited with ruthenium red or depleted with ryanodine, or when calmodulin antagonists or CaM kinase II inhibitors were present. 5. These results provide evidence that activation of an ionotropic glutamate receptor on catfish cone horizontal cells is linked to calcium release from ryanodine-sensitive intracellular calcium stores and modulation of the L-type calcium current activity. Inhibition of this calcium current directly or indirectly involves calmodulin and CaM kinase II and represents a possible mechanism used by horizontal cells to affect response properties of these cells.
Authors:
C L Linn; A C Gafka
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of physiology     Volume:  535     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2001 Aug 
Date Detail:
Created Date:  2001-08-16     Completed Date:  2001-11-01     Revised Date:  2013-06-09    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  47-63     Citation Subset:  IM    
Affiliation:
Western Michigan University, Department of Biological Sciences, 1903 W. Michigan Avenue, Kalamazoo, MI 49008, USA. clinn@unix.cc.wmich.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Caffeine / antagonists & inhibitors,  pharmacology
Calcium / metabolism*,  pharmacology*
Calcium Channels / drug effects,  physiology*
Calmodulin / metabolism
Catfishes
Dose-Response Relationship, Drug
Electric Conductivity
Excitatory Amino Acid Agonists / pharmacology
Inositol 1,4,5-Trisphosphate / metabolism
Intracellular Membranes / metabolism
Kainic Acid / antagonists & inhibitors,  pharmacology
Receptors, Glutamate / metabolism*
Retina / physiology*
Ruthenium Red / pharmacology
Ryanodine / pharmacology
Grant Support
ID/Acronym/Agency:
EY-11133/EY/NEI NIH HHS
Chemical
Reg. No./Substance:
0/Calcium Channels; 0/Calmodulin; 0/Excitatory Amino Acid Agonists; 0/Receptors, Glutamate; 11103-72-3/Ruthenium Red; 15662-33-6/Ryanodine; 487-79-6/Kainic Acid; 58-08-2/Caffeine; 7440-70-2/Calcium; 85166-31-0/Inositol 1,4,5-Trisphosphate
Comments/Corrections

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


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