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RISS 인기검색어
- 검색키워드
- 저자 : Herbison A. E. (검색결과 3 건)
- 무료
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Han, S.-K.,Lee, K.,Bhattarai, J. P.,Herbison, A. E. Blackwell Publishing Ltd 2010 Journal of neuroendocrinology Vol.22 No.3
<P>There is substantial evidence for a role of the neuropeptide gonadotrophin-releasing hormone (GnRH) in the regulation of GnRH neurone secretion but how this is achieved is not understood. We examined here the effects of GnRH on the electrical excitability and intracellular calcium concentration ([Ca<SUP>2+</SUP>]<SUB>i</SUB>) of GnRH neurones in intact adult male and female mice. Perforated-patch electrophysiological recordings from GnRH-green fluorescent protein-tagged GnRH neurones revealed that 3 n<SMALL>M</SMALL>–3 &mgr;<SMALL>M</SMALL> GnRH evoked gradual approximately 3 mV depolarisations in membrane potential from up to 50% of GnRH neurones in male and female mice. The depolarising effect of GnRH was observed on approximately 50% of GnRH neurones throughout the oestrous cycle. However, at pro-oestrus alone, GnRH was also found to transiently hyperpolarise approximately 30% of GnRH neurones. Both hyperpolarising and depolarising responses were maintained in the presence of tetrodotoxin. Calcium imaging studies undertaken in transgenic GnRH-pericam mice showed that GnRH suppressed [Ca<SUP>2+</SUP>]<SUB>i</SUB> in approximately 50% of GnRH neurones in dioestrous and oestrous mice. At pro-oestrus, 25% of GnRH neurones exhibited a suppressive [Ca<SUP>2+</SUP>]<SUB>i</SUB> response to GnRH, whereas 17% were stimulated. These results demonstrate that n<SMALL>M</SMALL> to &mgr;<SMALL>M</SMALL> concentrations of GnRH exert depolarising actions on approximately 50% of GnRH neurones in males and females throughout the oestrous cycle. This is associated with a reduction in [Ca<SUP>2+</SUP>]<SUB>i</SUB>. At pro-oestrus, however, a further population of GnRH neurones exhibit a hyperpolarising response to GnRH. Taken together, these studies indicate that GnRH acts predominantly as a neuromodulator at the level of the GnRH cell bodies to exert a predominant excitatory influence upon GnRH neurones in intact adult male and female mice.</P>
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Clarkson, J.,Han, S.K.,Liu, X.,Lee, K.,Herbison, A.E. North-Holland 2010 Molecular and cellular endocrinology Vol.324 No.1
Studies undertaken in many species indicate that kisspeptin-Gpr54 signaling is essential for the activation of gonadotropin-releasing hormone (GnRH) neurons to bring about puberty. Investigations in transgenic mouse models, in particular, have highlighted the importance of kisspeptin signaling at the level of the GnRH neuron itself in this process. This review aims to highlight current understanding of the neurobiological mechanisms underlying the kisspeptin activation of postnatal GnRH neurons. The three key features of the kisspeptin-Gpr54-GnRH neuron axis leading up to puberty are (i) the expression of adult-like levels of Gpr54 mRNA in GnRH neurons well in advance of puberty, (ii) a modest increase in the electrical response of GnRH neurons to Gpr54 activation across postnatal development and (iii), the ''sudden'' appearance of kisspeptin fibers surrounding GnRH neuron cell bodies/proximal dendrites just prior to puberty onset. These kisspeptin fibers are likely to originate from the kisspeptin population located in the rostral periventricular region of the third ventricle (RP3V). Together, available data suggest that the key step in the kisspeptin control of puberty lies in the control of kisspeptin synthesis within RP3V kisspeptin neurons that innervate GnRH neurons. This has recently been shown to be dependent upon circulating estradiol concentrations. As such, we propose that RP3V kisspeptin neurons represent a critical estradiol-dependent amplification mechanism brought into play relatively late in pubertal development to activate GnRH neurons and complete the process of puberty onset. Subsequently, in the adult female, this same circuitry is used to activate GnRH neurons to generate the cyclical preovulatory GnRH/LH surge.
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