Damage to the perirhinal cortex exacerbates memory impairment following lesions to the hippocampal formation.

نویسندگان

  • S Zola-Morgan
  • L R Squire
  • R P Clower
  • N L Rempel
چکیده

Recent work has been directed at identifying the critical components of the medial temporal lobe that, when damaged, produce severe memory impairment. The H+A+ lesion includes the hippocampal formation, the amygdala, and the adjacent entorhinal, parahippocampal, and perirhinal cortices. A more restricted medial temporal lobe lesion that includes the hippocampal formation and parahippocampal cortex (the H+ lesion) produces less severe memory impairment. Previous work demonstrated that extending the H+ lesion forward to include the amygdala did not exacerbate the impairment. Here, we tested the hypothesis that extending the H+ lesion forward to include the perirhinal cortex (the H++ lesion), but sparing the amygdala, should produce a more severe memory impairment and one that would approximate the level of memory impairment associated with the H+A+ lesion. Monkeys with the H++ lesion were severely impaired on two of three amnesia-sensitive tasks (delayed nonmatching to sample and delayed retention of object discrimination). On the third amnesia-sensitive task (concurrent discrimination learning), two of the monkeys in the H++ group obtained poorer scores than all seven normal monkeys, although the overall group comparison was not significant. The memory impairment following H++ damage was more severe overall than the impairment associated with the H+ lesion and approached the level of impairment associated with the H+A+ lesions. Quantitative measurement of damage in each anatomical component of the lesion indicated that the perirhinal cortex was the only brain region that was more extensively damaged in the H++ group than in the H+ group. These findings emphasize the importance of the perirhinal cortex in the anatomy of the medial temporal lobe memory system.

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عنوان ژورنال:
  • The Journal of neuroscience : the official journal of the Society for Neuroscience

دوره 13 1  شماره 

صفحات  -

تاریخ انتشار 1993