التفاصيل البيبلوغرافية
| العنوان: |
FXYD1, a Modulator of Na+,K+-ATPase Activity, Facilitates Female Sexual Development by Maintaining Gonadotrophin-Releasing Hormone Neuronal Excitability. |
| المؤلفون: |
Garcia-Rudaz, C., Deng, V., Matagne, V., Ronnekleiv, O. K., Bosch, M., Han, V., Percy, A. K., Ojeda, S. R. |
| المصدر: |
Journal of Neuroendocrinology; Feb2009, Vol. 21 Issue 2, p108-122, 15p, 2 Diagrams, 1 Chart, 5 Graphs |
| مصطلحات موضوعية: |
HOMEOSTASIS, ENDOCRINE glands, HYPOTHALAMUS, PUBERTY, NEUROPLASTICITY |
| مستخلص: |
The excitatory tone to gonadotrophin-releasing hormone (GnRH) neurones is a critical component underlying the pubertal increase in GnRH secretion. However, the homeostatic mechanisms modulating the response of GnRH neurones to excitatory inputs remain poorly understood. A basic mechanism of neuronal homeostasis is the Na+,K+-ATPase-dependent restoration of Na+ and K+ transmembrane gradients after neuronal excitation. This activity is reduced in a mouse model of Rett syndrome (RTT), a neurodevelopmental disorder in which expression of FXYD1, a modulator of Na+,K+-ATPase activity, is increased. We now report that the initiation, but not the completion of puberty, is advanced in girls with RTT, and that, in rodents, FXYD1 may contribute to the neuroendocrine regulation of female puberty by modulating GnRH neuronal excitability. Fxyd1 mRNA abundance reaches maximal levels in the female rat hypothalamus by the fourth postnatal week of life (i.e., around the time when the mode of GnRH secretion acquires an adult pattern of release). Although Fxyd1 mRNA expression is low in the hypothalamus, approximately 50% of GnRH neurones contain Fxyd1 transcripts. Whole-cell patch recording of GnRH–EGFP neurones revealed that the neurones of Fxyd1-null female mice respond to somatic current injections with a lower number of action potentials than wild-type cells. Both the age at vaginal opening and at first oestrous were delayed in Fxyd1 −/− mice, but adult reproductive capacity was normal. These results suggest that FXYD1 contributes to facilitating the advent of puberty by maintaining GnRH neuronal excitability to incoming transsynaptic stimulatory inputs. [ABSTRACT FROM AUTHOR] |
|
Copyright of Journal of Neuroendocrinology is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) |
| قاعدة البيانات: |
Complementary Index |
Full Text Finder