1988 Fiscal Year Final Research Report Summary
Molecular mechanisms invovlved in sexual differentiation of the rat brain
| Project/Area Number |
62570071
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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 |
環境生理学(含体力医学･栄養生理学)
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| Research Institution | HIROSAKI UNIVERSITY (1988)
Niigata University (1987) |
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Principal Investigator |
SAKUMA Yasuo Professor, Department of Physiology I, Hirosaki University School of Medicine, 医学部, 教授 (70094307)
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| Co-Investigator(Kenkyū-buntansha) |
AKAISHI Takao Lecturer, Department of Physiology II, Niigata University School of Medicine, 医学部, 講師 (70018951)
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| Project Period (FY) |
1987 – 1988
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| Keywords | Lordosis / Midbrain central gray / Nerve growth factor / Sexual dimorphism / Testosterone / 中脳中心灰白質 / テストステロン / ロード-シス / 逆行性興奮 / 活動電位 / 腹内側核 |
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| Research Abstract |
Injection of antibody to nerve growth factor into the cerebral lateral ventricle blocked testosterone-induced behavioral defeminization of neonatal female rat. When tested as adults following ovariectomy and the combined estrogen-progesterone treatment, the injected animals showed a significantly higher lordosis quotient than the testosterone-treated, normal rebbit serum infused controls. Failure of vaginal opening and clitoral enlargement manifested the well-documented masculinizing effect of testosterone on the genitalia in the experimental as well as the control animals. Estrogen-sensitivity of hypothalamic neurons which are responsible for the induction of lordosis was retained in the experimental animals. Recordings of the antidromic action potentials from neurons in the ventromedial nucleus of the hypothalamus following stimulation of the midbrain central gray revealed that estrogen decreased the antidromic activation threshold and shortened the absolute refractory period of th e hypothalamic efferents along with the estrogen-induced behavioral activation in the experimental animals. In the control group, the estrogen-induced neuronal activation was lost altogether with the behavioral activation.
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