Document Detail


Dynamics of the actions of tetrahydro-9-aminoacridine and 9-aminoacridine on glutamatergic currents: concentration-jump studies in cultured rat hippocampal neurons.
MedLine Citation:
PMID:  7507997     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The actions of 1,2,3,4-tetrahydro-9-aminoacridine (THA) and 9-aminoacridine (9-AA) on glutamatergic receptors were studied using the whole-cell and outside-out variants of the patch-clamp technique. Typically, either N-methyl-D-aspartate (NMDA) or kainate alone or combined with various concentrations of THA or 9-AA was applied via a U tube to activate whole-cell currents. Other superfusion techniques were also used. THA (25-50 microM) and 9-AA (10-25 microM) reduced the peak and steady-state amplitudes of NMDA-activated whole-cell inward currents and had no significant effect on outward currents. At higher concentrations, these agents produced a delayed current peak in addition to a further depression of the current size. A delayed current peak was a high-amplitude current peak delayed in relation to the time course of control currents. THA and 9-AA were much less potent in blocking kainate-activated currents. Also, the blockade of kainate currents was voltage independent, and no delayed current peak was generated. With the same superfusion method, the antagonists APV (DL-2-amino-5-phosphonovaleric acid) and Mg++ were tested independently of THA or 9-AA and were found not to produce delayed current peaks or NMDA-activated whole-cell currents. Bath perfusion of THA (250 microM) abolished the delayed current peaks produced by pulse application of NMDA and THA, whereas bath perfusion of the competitive blocker APV did not have this effect. High concentrations of glycine (10 microM) did not alter THA's blocking effects or the production of delayed current peaks.(ABSTRACT TRUNCATED AT 250 WORDS)
Authors:
A C Costa; E X Albuquerque
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of pharmacology and experimental therapeutics     Volume:  268     ISSN:  0022-3565     ISO Abbreviation:  J. Pharmacol. Exp. Ther.     Publication Date:  1994 Jan 
Date Detail:
Created Date:  1994-03-10     Completed Date:  1994-03-10     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0376362     Medline TA:  J Pharmacol Exp Ther     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  503-14     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Experimental Therapeutics, University of Maryland, School of Medicine, Baltimore.
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MeSH Terms
Descriptor/Qualifier:
Aminacrine / pharmacology*
Animals
Cells, Cultured
Dose-Response Relationship, Drug
Hippocampus / cytology,  drug effects*,  metabolism,  physiology
Ion Channels / drug effects
Kainic Acid / pharmacology
N-Methylaspartate / pharmacology
Neurons / drug effects*,  metabolism,  physiology
Rats
Receptors, Glutamate / drug effects*
Tacrine / pharmacology*
Chemical
Reg. No./Substance:
0/Ion Channels; 0/Receptors, Glutamate; 321-64-2/Tacrine; 487-79-6/Kainic Acid; 6384-92-5/N-Methylaspartate; 90-45-9/Aminacrine

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


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