Document Detail


Trifluoperazine and dibucaine-induced inhibition of glutamate-induced mitochondrial depolarization in rat cultured forebrain neurones.
MedLine Citation:
PMID:  9384493     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
1. Glutamate receptor activation has been previously shown to result in mitochondrial depolarization and activation of the mitochondrial permeability transition pore in cultured neurones. In this study, we characterized the effects of two putative permeability transition inhibitors, namely trifluoperazine and dibucaine, on mitochondrial depolarization in rat intact, cultured forebrain neurones. 2. Permeability transition was monitored by following mitochondrial depolarization in neurones loaded with the mitochondrial membrane potential-sensitive fluorescent indicator, JC-1. Trifluoperazine (10 20 microM) and dibucaine (50-100 microM) inhibited or delayed the onset of glutamate-induced permeability transition. 3. We also investigated the effects of trifluoperazine and dibucaine on neuronal recovery from glutamate-induced Ca2+ loads. Trifluoperazine affected Ca2+ recovery in a manner similar to the mitochondrial Na+/Ca2+ exchange inhibitor, CGP-37157, while dibucaine had no apparent effect on Ca2+ recovery. Therefore, inhibition of permeability transition does not appear to be involved in Ca2+ recovery from glutamate-induced Ca2+ loads. 4. Trifluoperazine and dibucaine did not inhibit [3H]-dizocilpine binding at the concentrations that prevented mitochondrial depolarization. 5. These studies suggest that trifluoperazine and dibucaine inhibit permeability transition in intact neurones. Trifluoperazine also appears to inhibit mitochondrial Na+/Ca2+ exchange. These drugs should prove to be valuable tools in the further study of the role of mitochondrial permeability transition in glutamate-induced neuronal death.
Authors:
K R Hoyt; T A Sharma; I J Reynolds
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  British journal of pharmacology     Volume:  122     ISSN:  0007-1188     ISO Abbreviation:  Br. J. Pharmacol.     Publication Date:  1997 Nov 
Date Detail:
Created Date:  1998-09-24     Completed Date:  1998-09-24     Revised Date:  2008-11-20    
Medline Journal Info:
Nlm Unique ID:  7502536     Medline TA:  Br J Pharmacol     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  803-8     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Pittsburgh School of Medicine, PA 15261, U.S.A.
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MeSH Terms
Descriptor/Qualifier:
Animals
Benzimidazoles
Calcium / metabolism
Carbocyanines
Cells, Cultured
Clonazepam / analogs & derivatives,  pharmacology
Dibucaine / metabolism,  pharmacology*
Dizocilpine Maleate / metabolism
Fluorescent Dyes
Fluorometry
Glutamic Acid / physiology*
Membrane Potentials / drug effects
Mitochondria / drug effects*,  physiology
Neurons / cytology,  drug effects*
Prosencephalon / cytology,  drug effects*,  metabolism
Rats
Rats, Sprague-Dawley
Sodium-Calcium Exchanger / antagonists & inhibitors
Thiazepines / pharmacology
Trifluoperazine / metabolism,  pharmacology*
Grant Support
ID/Acronym/Agency:
NS 34138/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Benzimidazoles; 0/Carbocyanines; 0/Fluorescent Dyes; 0/Sodium-Calcium Exchanger; 0/Thiazepines; 117-89-5/Trifluoperazine; 1622-61-3/Clonazepam; 21527-78-6/5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine; 56-86-0/Glutamic Acid; 7440-70-2/Calcium; 75450-34-9/CGP 37157; 77086-22-7/Dizocilpine Maleate; 85-79-0/Dibucaine

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


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