頁籤選單縮合
題 名 | Neuroendocrine Signals in the Regulation of Gonadotropin-releasing Hormone Secretion |
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作 者 | Francis Pau,Kwok-yuen; Spies,Harold G.; | 書刊名 | 中國生理學雜誌 |
卷 期 | 40:4 1997.12[民86.12] |
頁 次 | 頁181-196 |
分類號 | 361.1 |
關鍵詞 | Norepinephrine; Norepinephrine transporter; Tyrosine hydroxylase; Gonadotropin-releasing hormone; Neuropeptide Y; Interleukin-1; Opioid peptides; Hypothalamus; Locus coeruleus; Monkey; Rabbit; |
語 文 | 英文(English) |
英文摘要 | Gonadotropin-releasing hormone (GnRH) is a key bypothalamic peptide that controls thesecretion of pituitary gonadotropins, particularly luteinizing hormone (LH), and hence gonadal function.Hypothalamic GnRH is released in a pulsatile manner. In the female, the pattern of GnRH pulses, i.e.,pulse frequency and amplitude, varies during different reproductive stages and among different species.Several central and peripheral signals modulate GnRH neuronal activities. Some of these signals arestimulatory to GnRH release, e.g., norepinephrine (NE) and neuropeptide Y (NPY); some are inhibitory,e.g., fi-endorphin and interleukin-1; others are both stimulatory and inhibitory, e.g., estradiol-17B (E2).The neuronal structures and chemical interactions that result in pulsatile GnRH release remainunresolved. However, the core of the so- called 'GnRH pulse-generator' likely involves NE and NEtransporter (NET, the protein for pre-synaptic re-uptake of NE). Both secretion and re-uptake of NEmay determine hypothalamic NE availability. Many of the GnRH-stimulating and GnRH-inhibitingsignals may influence the 'pulse-generator' by acting on GnRH neurons as second level signals.Hypothalamic GnRH is also released in a "surge" manner that is triggered either by increasing levels ofcirculating steroids (E2 and progesterone) during the preovulatory period in spontaneous-ovulatingspecies, or by coitus in induced-ovulating animals. The sequential steps and mechanisms by which theGnRH surge occurs after E2 or coitus are not clear. However, it is unlikely that the E2 or coital stimuliact directly on GnRH neurons; E2 receptors have not been found in GnRH cells whereas coital signalsmust stop in the brainstem before they reach the hypothalamus. The brainstem may be an extra1hypothalamic site where both E2 and coital stimuli are transformed into GnRH-stimulating signals. Onesuch signal may be NE whose brainstem cell bodies send terminals into the hypothalamus. Evidencefrom our laboratory suggests that a hypothalamic NE surge occurs at the time of the preovulatory GnRHsurge in both the monkey and rabbit. Moreover, gene expression of both tyrosine hydroxylase (the rate1limiting enzyme for NE synthesis) and NET (the rate-limiting factor for synaptic NE transmission) in thebrainstem increases after E2 in the monkey and after coitus in the rabbit. Other hypothalamic and/orbrainstem signals, i.e., NPY, galanin, fi-endorphin, nitrous oxide and gamma aminobutyric acid, arelikely involved in generating, maintaining and/or modulating the GnRH surge process. A betterunderstanding of the up-stream GnRH-regnlating signals will help improve treatments for manyreproductive disorders associated with stress, obesity, infection and aging. |
本系統中英文摘要資訊取自各篇刊載內容。