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| Research article summary (published 30 May 2004): |
Retrograde amnesia induced by drugs acting on different molecular systems.
Full Abstract
The gamma aminobutyric acid-A (GABA-sub(A)) agonist, muscimol, the glutamate N-methyl-D-aspartate (NMDA) receptor antagonist, D-2-amino-5-phosphonopentanoic acid (AP5), and the inhibitor of the extracellularly regulated kinases (ERKs), UO 126, cause retrograde amnesia when administered to the hippocampus. In the present study, the authors found that they all cause retrograde amnesia for 1-trial inhibitory avoidance, not only when infused into the dorsal CA1 region of the hippocampus, but also when infused into the basolateral amygdala or the entorhinal, parietal, and posterior cingulate cortices. The posttraining time course of the effect of each drug was, however, quite different across brain structures. Thus, in all of them, NMDA receptors and the ERK pathway are indispensable for memory consolidation, and GABA-sub(A) receptor activation inhibits memory consolidation: but in each case, their influence is interwoven differently. ((c) 2004 APA, all rights reserved)
Author information
Author/s: Rossato, Janine I (JI); Bonini, Juliana S (JS); Coitinho, Adriana S (AS); Vianna, Monica R M (MR); Medina, Jorge H (JH); Cammarota, Martín (M); Izquierdo, Iván (I);
Affiliation: Centro de Memoria, Departamento de Bioquimica, Institute de Ciencias Basicas da Saude, Universidade Federal do Rio Grande do Sul, Ramiro Barcellos 2600-Anexo, 90035-003 Porto Alegre, RS, Brazil.
Journal and publication information
Publication Type: Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
Journal: Behavioral neuroscience (Behav Neurosci), published in United States. (Language: eng)
Reference: 2004-Jun; vol 118 (issue 3) : pp 563-8
Dates: Created 2004/06/03; Completed 2004/07/19; Revised 2006/11/15;
PMID: 15174933, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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