Actions of ethanol on brain excitatory amino acid receptor activation at puberty /
The onset of female puberty requires a complex interplay of
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| Format: | Thesis Book |
| Language: | English |
| Published: |
[Place of publication not identified] :
[publisher not identified] ;
1994.
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| Subjects: | |
| Online Access: | http://proxy.library.tamu.edu/login?url=http://proquest.umi.com/pqdweb?did=741965931&sid=1&Fmt=2&clientId=2945&RQT=309&VName=PQD |
| Summary: | The onset of female puberty requires a complex interplay of hypothalamic-pituitary-ovarian interactions. Recently, information has been gathered showing that activation of hypothalamic N-methyl-D-aspartate (NMDA) receptors is required for this event to occur [1-3]. Ethanol (ETOH) administration during the peripubertal period can delay onset of female puberty in the rat [4]. In the present study, we examined possible mechanisms by which N-methyl-DL-aspartic acid (NMA) acts to induce luteinizing hormone releasing hormone (LHRH) release at the time of puberty and whether ETOH could affect a number of indices of puberty related to excitatory amino acid (EAA) activation of the NMDA receptor. Our data show that ETOH dose dependently blocks the NMA- induced release of LHRH in vitro. Additionally, we've shown that NMA is significantly more effective at inducing luteinizing hormone (LH) release at first proestrus and that a single acute dose of ETOH can block this action of NMA. Importantly, we showed that ETOH attenuates NMA's ability to induce puberty. Furthermore, we have shown that expression of the NMDA receptor increases during the late juvenile period in the medial basal hypothalamic and preoptic area (POA) and again in the POA at the time of first proestrus. However, short-term ETOH exposure did not affect expression of this receptor in late prepubertal female rats, indicating that ETOH must block or mask the receptor by some other mechanism. Recent evidence indicates that nitric oxide (NO) mediates the release of LHRH induced by EAAs and by the norepinephrine- (NE) prostaglandin E2 (PGE2) pathway [5,6], therefore, we examined whether NMA acts to induce PGE2 release and how ETOH might affect this system. Our results indicate that NMA can induce a significant increase in PGE2 release in vitro and PGE2and LHRH induced by sodium nitroprusside (SNP), a NO donor. The present results further demonstrate that the activation of the NMDA receptor plays a crutial role in the onset of female puberty, and suggest that ETOH can interfere with the pubertal process via an action at the hypothalamic level to diminish EAA-activated LHRH secretion. |
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| Item Description: | Vita. "Major Subject: Veterinary Anatomy". |
| Physical Description: | x, 84 leaves : illustrations ; 28 cm. Issued also on microfiche from University Microfilms Inc. |
| Bibliography: | Includes bibliographical references. |