Paper Information

Title: 

EFFECT OF BLOCKADE OF DORSAL HIPPOCAMPAL NMDA RECEPTORS ON ETHANOL STATE-DEPENDENT LEARNING

Type: POSTER
Author(s): SHARIFI KH.*,REZAYOF A.,RASOULI Y.,ZARINDAST M.R.
 
 *SCHOOL OF BIOLOGY, UNIVERSITY COLLEGE OF SCIENCE, UNIVERSITY OF TEHRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: Some studies have shown that ethanol administration has impairing effects on learning and memory processes by disrupting activity in the hippocampus. Considering the dorsal hippocampus is a brain region that is particularly sensitive to ethanol and dorsal hippocampal NMDA receptors are involved in the modulation of memory, in the present study, the effects of intra-hippocampal CA1 injections of the NMDA receptors antagonist, DAP-5 on ethanol state-dependent learning has been investigated in mice.
Methods: A single-trial step-down passive avoidance task was used for the assessment of memory retention in adult male NMRI mice. Animals were bilaterally cannulated in the CA1 regions by stereotaxic instrument, and were allowed to recover 1-week before training.
Results: Post-training intraperitoneal administration of the different doses of ethanol (0.5-2 g/kg) dose dependently induced impairment of memory retention. Pre-test administration of ethanol (2 g/kg) induced state-dependent retrieval of the memory acquired under post-training ethanol (2 g/kg) influence. Intra-CA1 administration of the NMDA receptors antagonist, DAP-5 (0.5-1.5 µg/mouse) alone cannot affect memory retention. Pre-test injection of DAP-5 (0.5-1.5 µg/mouse) into the CA1 regions, 5 min before the administration of ethanol (2 g/kg), significantly inhibited ethanol state-dependent learning.
Conclusion: The present data demonstrate that memory and the processes of learning in animals can be affected by ethanol and that ethanol produces state-dependent memory. Furthermore, these findings implicate the involvement of a glutamatergic mechanism in ethanol state-dependent learning through the NMDA receptors of the CA1 region of dorsal hippocampus.

 
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