| Budget Amount *help |
¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 1990: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1989: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1988: ¥700,000 (Direct Cost: ¥700,000)
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| Research Abstract |
The inferotemporal cortex (IT) of the monkey is accepted as a focus for pattern perception and visual memory. The IT functions were demonstrated to exclusively depend on the visual information from the striate cortex. In addition, the visual information does not directly reach IT but via the centrallateral prestriate cortex (CLPS) that represents central visual field. In the present study, we examined whether lesions limited to CLPS produce visual impairment similar to that following IT lesions. Nine rhesus and Japanese monkeys were used, divided into CLPS and IT lesion groups and normal control group. Monkeys were preoperatively trained on a pattern discrimination task and tested on its postoperative retention (30 trials/day with 4000-trial- limit). Then, monkeys were trained on visual memory tasks : serial and concurrent object discrimination tasks (30-60 trials/day for serial task and 48 trials/day for concurrent task) and a trial unique delayed matching to sample task (DMTS) (20 trials/day with 1000-trial-limit). After learning DMTS with basic 10 second delay, monkeys were tested with longer delays (for 100 trials for each 30 second and 60 second delays, 10 trials/day). CLPS group showed pattern discrimination deficits as severe as those of IT group. On visual memory tasks, however, deficits of CLPS groups were less severe than deficits of IT group. The posterior and the anterior parts of IT (areas TEO and TE, respectively) are more closely involved in pattern perception and in visual memory, respectively. Therefore, the results of pattern discrimination task support the idea that CLPS is the major relay area of visual information from the striate cortex to area TEO. The moderate deficits following CLPS lesions on visual memory tasks suggests a possibility that wider prestriate lesions are necessary to produce memory deficits similar to those following area TE lesions or other relay areas to area TE exist.
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