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Cerebral Cortex Advance Access originally published online on July 21, 2004
Cerebral Cortex 2005 15(4):403-408; doi:10.1093/cercor/bhh143
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Cerebral Cortex V 15 N 4 © Oxford University Press 2004; all rights reserved

Degradation of Signal Timing in Cortical Areas V1 and V2 of Senescent Monkeys

Yongchang Wang1,2,3, Yifeng Zhou2, Yuanye Ma3 and Audie G. Leventhal1,2

1 Department of Neurobiology & Anatomy, University of Utah School of Medicine, Salt Lake City, UT 84132, USA, 2 School of Life Science, University of Science and Technology of China, Hefei, Anhui 230027, China and 3 Laboratory of Primate Cognitive Neuroscience, Kunming Institute of Zoology, Chinese Academy of Science, Kunming, Yunnan 650223, China

Addressed correspondence to Audie G. Leventhal, Department of Neurobiology & Anatomy, University of Utah School of Medicine, Salt Lake City, UT 84132, USA. Email: audie.leventhal{at}m.cc.utah.edu.

Senescence in monkeys results in a degradation of the functional properties of cortical cells as well as prolonged hyperactivity. We have now compared the spontaneous and visually evoked activity levels, as well as the visual response latencies of cells in cortical areas V1 and V2 of young and very old monkeys. We found that V1 cells within layer 4 exhibit normal latencies. In contrast, in other parts of V1 and throughout V2 hyperactivity in old monkeys is accompanied by dramatic delays in both the intracortical and intercortical transfer of information. Extrastriate cortex (area V2) is affected more severely than striate cortex (V1). Delayed information processing in cerebral cortex should contribute to the declines in cortical function that accompany old age.

Key Words: degradation • latency • senescent monkeys • visual information processing • visual cortex


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