Opposite relationship of hippocampal and rhinal cortex damage to delayed nonmatching-to-sample deficits in monkeys.
Three recent studies in macaque monkeys that examined the effects on memory of restricted hippocampal lesions (Murray and Mishkin, J Neurosci 1998;18:6568-6582; Beason-Held et al., Hippocampus 1999;9:562-574; Zola et al., J Neurosci 2000;20:451-463) differed in their conclusions about the involvement of the hippocampus in recognition memory. Because these experiments used a common behavioral procedure, trial-unique visual delayed nonmatching-to-sample (DNMS), a quantitative synthesis ("meta-analysis") was performed to determine whether hippocampal lesions produced a reliable net impairment in DNMS performance, and whether this impairment was related to the magnitude of hippocampal damage. A similar analysis was performed on data from monkeys with perirhinal or rhinal cortex damage (Meunier et al., J Neurosci 1993;13:5418-5432; Buffalo et al., Learn Mem 1999;6:572-599). DNMS performance scores were transformed to d' values to permit comparisons across studies, and a loss in d' score, a measure of the magnitude of the recognition deficit relative to the control group, was calculated for each operated monkey. Two main findings emerged. First, the loss in d' following hippocampal damage was reliably larger than zero, but was smaller than that found after lesions limited to the perirhinal cortex. Second, the correlation of loss in d' with extent of hippocampal damage was large and negative, indicating that greater impairments were associated with smaller hippocampal lesions. This relationship was opposite to that between loss in d' and rhinal cortex damage, for which larger lesions were associated with greater impairment. These findings indicate that damage to the hippocampus and to the rhinal cortex affects recognition memory in different ways. Furthermore, they provide a framework for understanding the seemingly disparate effects of hippocampal damage on recognition memory in monkeys, and by extension, for interpreting the conflicting reports on the effects of such damage on recognition memory abilities in amnesic humans.
Baxter
M G
MG
Department of Psychology, Harvard University, Cambridge, Massachusetts 02138, USA. mbaxter@wjh.harvard.edu
Murray
E A
EA
D000818:Animals; D018728:Entorhinal Cortex / Q000473:pathology* / Q000503:physiopathology*; D006624:Hippocampus / Q000473:pathology* / Q000503:physiopathology*; D008251:Macaca; D008569:Memory Disorders / Q000503:physiopathology*; D011597:Psychomotor Performance