Object and spatial memory after neonatal perirhinal lesions in monkeys

• Type of Material: Article
• Authors: Alison R Weiss, Yerkes National Primate Research Center; Jocelyne Bachevalier, Emory University
• Language: English
• Date: 2015-11-23
• Publisher: Elsevier
• Publication Version: Final Published Version
• Copyright Statement: ©2015, The Authors. Published by Elsivier B.V.
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.bbr.2015.11.010
• Title of Journal or Parent Work: Behavioural Brain Research
• ISSN: 0166-4328
• Volume: 298
• Start Page: 210
• End Page: 217
• Grant/Funding Information: This work was supported by the National Institute of Mental Health (MH-58846 to JB and T32-HD071845 to ARW), the National Science Foundation (NSF-GRFP DGE-1444932 to ARW), and the National Center for Research Resources P51RR165, currently supported by the Office of Research Infrastructure Programs/OD P51OD11132.
• Keywords: developmental amnesia; memory span; excitotoxic lesion; recognition; rhesus macaque; medial temporal lobe epilepsy
• Research Categories: Psychology, Cognitive; Biology, Neuroscience; Biology, Zoology

Abstract

The contribution of the perirhinal cortex (PRh) to recognition memory is well characterized in adults, yet the same lesions have limited effect on recognition of spatial locations. Here, we assessed whether the same outcomes will follow when perirhinal lesions are performed in infancy. Monkeys with neonatal perirhinal (Neo-PRh) lesions and control animals were tested in three operant recognition tasks as they reached adulthood: Delayed Nonmatching-to-Sample (DNMS) and Object Memory Span (OMS), measuring object recognition, and Spatial Memory Span (SMS), measuring recognition of spatial locations. Although Neo-PRh lesions did not impact acquisition of the DNMS rule, they did impair performance when the delays were extended from 30s to 600s. In contrast, the same neonatal lesions had no impact on either the object or spatial memory span tasks, suggesting that the lesions impacted the maintenance of information across longer delays and not memory capacity. Finally, the magnitude of recognition memory impairment after the Neo-PRh lesions was similar to that previously observed after adult-onset perirhinal lesions, indicating minimal, or no, functional compensation after the early PRh lesions. Overall, the results indicate that the PRh is a cortical structure that is important for the normal development of mechanisms supporting object recognition memory. Its contribution may be relevant to the memory impairment observed with human cases of temporal lobe epilepsy without hippocampal sclerosis, but not to the memory impairment found in developmental amnesia cases.