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dc.contributor.authorSmyth, Catherine Elizabeth.en_US
dc.date.accessioned2014-10-21T12:37:01Z
dc.date.available1995
dc.date.issued1995en_US
dc.identifier.otherAAINN05303en_US
dc.identifier.urihttp://hdl.handle.net/10222/55071
dc.descriptionN-methyl-D-aspartic acid (NMDA) subtype receptors are important in regulating sexual maturation. Daily treatment with NMDA (20 mg/kg; s.c.) from 24 days of age advances first ovulation in immature female rats while daily injections of gonadotropin releasing hormone (GnRH; 5 ng/100 g) do not. This suggests that NMDA alters hypothalamic control, not directly related to LH secretion. There is a critical period for effectiveness as daily injections from day 16 to 20 or immediately preceding spontaneous first ovulation do not induce precocious puberty. An LH dose-response curve for NMDA (P28) demonstrates that in rats previously treated with NMDA (P24 to P27), the LH response is lower than in rats previously treated with saline (P24 to P27). The site of action of NMDA was localized by c-fos immunoreactivity (FLI) which was identified in a dose-dependent manner in circumventricular organs (CVOs) following treatment with NMDA or monosodium glutamate (MSG). In this second model of precocious puberty, the arcuate nucleus (ARCN) of MSG-treated neonatal rats showed a dose- and age-dependent increase in FLI. NMDA- but not MSG-induced FLI in neonates was blocked by MK-801 even though MK-801 has been shown to prevent MSG-induced early puberty.en_US
dc.descriptionPrecocious maturation may be mediated through focal lesions in the ARCN. The stress protein, HSP72, increased in an NMDA dose-dependent manner in the ARCN of female rats. HSP72-like immunoreactivity (-li) peaked between 12 and 18 hrs. and disappeared 7 days post-treatment and was not evident in neonatal rats (P2 to 10) at any time following MSG- or NMDA-treatment.en_US
dc.descriptionGrowth factors are also believed to regulate puberty. High levels of bFGF mRNA were localized by reverse transcription polymerase chain reaction (RT-PCR) in rat hypothalamus and were found to decrease 40% at VO (P29) in NMDA-treated rats. Immunocytochemistry showed more bFGF-positive cells in the ARCN in NMDA-treated rats on P29; these fell significantly by P33.en_US
dc.descriptionThe data has shown that there is a critical time point where daily subcutaneous treatment with NMDA accelerates sexual maturation in the female rat. NMDA is acting on brain cells in the ARCN and other CVOs and may induce "stress" or injury in the ARCN. In addition, bFGF may be involved in the process leading to NMDA-induced precocious puberty.en_US
dc.descriptionThesis (Ph.D.)--Dalhousie University (Canada), 1995.en_US
dc.languageengen_US
dc.publisherDalhousie Universityen_US
dc.publisheren_US
dc.subjectBiology, Animal Physiology.en_US
dc.titleNMDA receptors and the neural control of puberty in female rats.en_US
dc.typetexten_US
dc.contributor.degreePh.D.en_US
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