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Interactions of spino-medullal ascending neural system and forebrain-hypothalamic structures in regulating gonadotropin release in female rats.

作者信息

Kawakami M, Ohno M N

出版信息

Acta Morphol Hung. 1983;31(1-3):117-36.

PMID:6414256
Abstract

The role of noradrenergic neurons originating in the lower brain stem with preoptic projection in controlling the preovulatory release of gonadotropins was investigated in female rats. Electrolytic lesions or diethyldithiocarbamate implantations in the ventrolateral part of the medulla oblongata (VLMO), but not in the dorsomedial part of the medulla oblongata, at 1100-1330 h on proestrus resulted in a blockade of the preovulatory release of LH, FSH and PRL as well as ovulation. Norepinephrine (NE) contents in the preoptic-anterior hypothalamic area at 1700-1800 h on proestrus were significantly reduced by VLMO lesions. Complete spinal transections at T3-T7, but not at T8-L5, of the spinal cord segments also blocked the preovulatory gonadotropin release and ovulation with significant reduction of NE contents in the preoptic-anterior hypothalamic area. Electrochemical stimulation of the suprachiasmatic part of the preoptic area (POSC) or NE injections into the third ventricle at 1400-1500 h on proestrus restored ovulation in animals with either VLMO lesions or complete spinal transections at T4-T5. Some neurons in the VLMO were antidromically activated by electrical stimulations of the POSC or the bed nucleus of stria terminalis (BST) in ovariectomized estradiol-primed rats. Generation of action potential of some of these neurons was facilitated or suppressed by estradiol administered ionophoretically. In proestrus rats, the number of neurons in the POSC and BST which responded to VLMO stimulations decreased significantly after the injection of phenoxybenzamine. The injection of pimozide and methysergide did not affect unit responses. These results suggest that noradrenergic neurons originating in the VLMO have stimulatory role in the induction of the preovulatory release of gonadotropins and that activities of these neurons are modulated by estradiol and spinal ascending neural input.

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