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Mei-Ling Ho and Jau-Nan Lee

Ovarian extracts of Long-Evans rats separated using high performance liquid chromatography (HPLC) were measured by radioimmunoassays (RIAs) for the presence of oxytocin and arginine vasopressin (AVP). The results showed that the ovary contains both, and that they are indistinguishable from the respective standard synthetic peptides. During the estrous cycle, the ovarian content of oxytocin was 10-fold higher (p<0.01) in estrus than in the other phases, while AVP was 16- and 25-fold higher (p<0.01) in metestrus than in the other phases. In contrast, the plasma levels of oxytocin showed no significant difference among the various phases of the estrous cycle. However, the plasma level of AVP level was significantly higher (p<0.01) in diestrus than in other phases. The present study thus strongly supports the hypothesis that both oxytocin and AVP can be produced by the ovary itself in the rat. The possible roles of oxytocin and AVP in the reproductive cycle are discussed.

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Chin Hsu, Jau-Nan Lee, Mei-Ling Ho, Bi-Hwa Cheng, Pi-Hseuh Shirley Li and John Yuh-Lin Yu

The purpose of this study was to examine whether N-methyl-D-aspartate affects the sexual receptivity of female rats. Monosodium L-glutamate was used as a neurotoxin to induce hypogonadal status. Matured normal and monosodium L-glutamate-treated rats were ovariectomized and implanted subcutaneously with estradiol capsules. One week later, lordosis responsiveness was observed before and 10 min after N-methyl-D-aspartate (40 mg/kg of BW, ip) administration. The results showed that N-methyl-D-aspartate caused a remarkable increase of lordosis quotient in control rats but not in monosodium L-glutamate-treated rats. Moreover, the possible action site of N-methyl-D-aspartate in the enhancement of receptivity was evaluated by the post-castrational LH rise, pituitary LH release in response to GnRH, and N-methyl-D-aspartate-evoked GnRH releasability. The results revealed that: (a) serum levels of LH in monosodium L-glutamate-treated rats were lower (p <0.01) than those of control rats after ovariectomy; (b) there was no significant difference of pituitary LH release responsiveness to GnRH test between two groups; and (c) N-methyl-D-aspartate-evoked LH release in monosodium L-glutamate-treated rats was similar to that in the control rats. In conclusion, N-methyl-D-aspartate may facilitate the sexual receptivity through stimulating GnRH release. The failure of N-methyl-D-aspartate in enhancing receptivity in monosodium L-glutamate-treated rats is probably due to the cellular damage by monosodium L-glutamate on specific areas responsible for lordosis.