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Retrograde and anterograde memory following selective damage to the dorsolateral entorhinal cortex.

Authors: Gervais NJBarrett-Bernstein MSutherland RJMumby DG


Affiliations

1 Center for Studies in Behavioral Neurobiology (CSBN), Department of Psychology, Concordia University, 7141 Sherbrooke Street West (SP-244), Montreal, Quebec H4B 1R6, Canada. Electronic address: Nicole.Gervais@concordia.ca.
2 Center for Studies in Behavioral Neurobiology (CSBN), Department of Psychology, Concordia University, 7141 Sherbrooke Street West (SP-244), Montreal, Quebec H4B 1R6, Canada. Electronic address: Meaganbbernstein@gmail.com.
3 Department of Neuroscience, Canadian Centre for Behavioural Neuroscience, University of Lethbridge, 4401 University Drive, Lethbridge, Alberta T1K 3M4, Canada. Electronic address: Robert.Sutherland@uleth.ca.
4 Center for Studies in Behavioral Neurobiology (CSBN), Department of Psychology, Concordia University, 7141 Sherbrooke Street West (SP-244), Montreal, Quebec H4B 1R6, Canada. Electronic address: David.Mumby@concordia.ca.

Description

Retrograde and anterograde memory following selective damage to the dorsolateral entorhinal cortex.

Neurobiol Learn Mem. 2014 Dec;116:14-26

Authors: Gervais NJ, Barrett-Bernstein M, Sutherland RJ, Mumby DG

Abstract

Anatomical and electrophysiological evidence suggest the dorsolateral entorhinal cortex (DLEC) is involved in processing spatial information, but there is currently no consensus on whether its functions are necessary for normal spatial learning and memory. The present study examined the effects of excitotoxic lesions of the DLEC on retrograde and anterograde memory on two tests of allocentric spatial learning: a hidden fixed-platform watermaze task, and a novelty-preference-based dry-maze test. Deficits were observed on both tests when training occurred prior to but not following n-methyl d-aspartate (NMDA) lesions of DLEC, suggesting retrograde memory impairment in the absence of anterograde impairments for the same information. The retrograde memory impairments were temporally-graded; rats that received DLEC lesions 1-3 days following training displayed deficits, while those that received lesions 7-10 days following training performed like a control group that received sham surgery. The deficits were not attenuated by co-infusion of tetrodotoxin, suggesting they are not due to disruption of neural processing in structures efferent to the DLEC, such as the hippocampus. The present findings provide evidence that the DLEC is involved in the consolidation of allocentric spatial information.

PMID: 25108197 [PubMed - indexed for MEDLINE]


Links

PubMed: https://www.ncbi.nlm.nih.gov/pubmed/25108197?dopt=Abstract