Format

Send to

Choose Destination
See comment in PubMed Commons below
Eur Neuropsychopharmacol. 2006 May;16(4):241-7. Epub 2005 Sep 19.

Hypofunction of the dorsal hippocampal NMDA receptors impairs retrieval of memory to partially presented foreground context in a single-trial fear conditioning in rats.

Author information

1
Department of Physiology, Division of Neurophysiology, Medical Faculty, University of Cukurova, 01330-Balcali, Adana, Turkey. emelik@cu.edu.tr

Abstract

In the present study, the effects of N-methyl-D-aspartate (NMDA) receptor antagonist, D,L-2-amino-5-phosphonopentanoic acid (AP5) bilaterally infused into the dorsal hippocampus (2.0 microl /5 microg), on the retrieval of fear memory to partial and whole foreground cues were evaluated by using a step-through passive avoidance and Pavlovian fear conditioning. In the both conditioning tasks, following a 30-s preshock exposure period to the shock-associated context, rats received a single shock in a foreground manner for fear memory exhibition by freezing. Rats with AP5 infusion 5 min before the retrieval tests showed profound freezing deficits either immediately or 48 h after the shock in the testing section of the passive avoidance chamber where foreground cues was partially presented. In the Pavlovian conditioning chamber where fear conditioning was tested in the whole of the context that was explicitly paired with the shock, AP5 rats in all infusion schedules exhibited robust freezing responses. These results showed that hypofunction of the hippocampal NMDA receptors impaired the retrieval of fear memory to partial, and not whole, foreground cues. This suggests that NMDA receptors of the hippocampus are involved in the formation of background context representations about foreground events when there is a deficit in perceiving certain sensory properties of the foreground retrieval cues.

PMID:
16176870
DOI:
10.1016/j.euroneuro.2005.07.008
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Support Center