1994 Fiscal Year Final Research Report Summary
Biopsychological study on learning deficits in chronic vitamin E-deficient rats
| Project/Area Number |
05610055
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
実験系心理学
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| Research Institution | University of Tsukuba |
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Principal Investigator |
ICHITANI Yukio Institute of Psychology, University of Tsukuba, Associate Professor, 心理学系, 助教授 (80176289)
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| Co-Investigator(Kenkyū-buntansha) |
IWASAKI Tsuneo Institute of Psychology, University of Tsukuba, Professor, 心理学系, 教授 (70092509)
FURUKAWA Satoshi School of Pharmacy, Hoshi University, Lecturer, 講師 (70229110)
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| Project Period (FY) |
1993 – 1994
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| Keywords | vitamin E / learning / memory / acetylcholine / rat |
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| Research Abstract |
We have already reported the possibility that chronic vitamin E deficiency causes learning impairment. In this study, we first investigated the biochemical changes of central nervous system mediating this learning impairment with special reference to the brain cholinergic neuron system, since this system has been shown related to learning and memory. Rats were fed vitamin E-deficient [VE (-)], -supplemented [VE (+)], or control food beginning after the age of 4 weeks until 24 months. At this time serum and brain vitamin E concentration was significantly different between 3 groups. Choline acetyltransferase and acetylcholinesterase activities measured as markers for brain cholinergic function were not affected by long-term vitamin E deficiency and supplementation in all brain regions measured. Thus results showed that chronic vitamin E deficiency did not lead to lower levels of activity in brain cholinergic enzymes.
Next we investigated the histological changes in the peripheral nervous system and behavioral changes in response to noxious stimulus. Rats were fed 3 kinds of diet mentioned above and they were tested with flight responses to electrical foot shock at the age of 9 months. Rats fed VE (-) diet showed significantly lower sensitivity to the foot shock compared with VE (+) and control groups. According to a histological observation of the spinal dorsal root ganglia, the number of neurons in VE (-) group was not different from that in other 2 groups. However, the location of satellite cells surrounding these neurons tended to be disordered. Thus our results suggest learning impairment in passive avoidance response caused by chronic vitamin E deficiency may partly come from the lower shock sensitivity associated with peripheral nervous system dysfunction.
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