| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Section of Endocrinology, Department of Pediatrics, University of Chicago, Chicago, Illinois 60637-1470
Address all correspondence and requests for reprints to: Daniel J. Spergel, Section of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Chicago, 5841 South Maryland Avenue, MC 1027, Chicago, Illinois 60637-1470. E-mail: dspergel{at}uchicago.edu.
The pubertal increase in GnRH secretion resulting in sexual maturation and reproductive competence is a complex process involving kisspeptin stimulation of GnRH neurons and requiring Ca2+ and possibly other intracellular messengers. To determine whether the expression of Ca2+ channels, or small-conductance Ca2+-activated K+ (SK) channels, whose activity reflects cytoplasmic free Ca2+ concentration, changes at puberty in GnRH neurons, Ca2+ and SK currents in GnRH neurons were recorded in brain slices of juvenile [postnatal day (P) 10–21], pubertal (P28–P42), and adult (
P56) male GnRH-green fluorescent protein transgenic mice using perforated-patch and whole-cell techniques. Ca2+ currents were inhibited by the Ca2+ channel blocker Cd2+ and showed marked heterogeneity but were on average similar in juvenile, pubertal, and adult GnRH neurons. SK currents, which were inhibited by the SK channel blocker apamin and enhanced by the SK and intermediate-conductance Ca2+-activated K+ channel activator 1-ethyl-2-benzimidazolinone, were also on average similar in juvenile, pubertal, and adult GnRH neurons. These findings suggest that whereas Ca2+ and SK channels may participate in the pubertal increase in GnRH secretion and there may be changes in Ca2+ or SK channel subtypes, overall Ca2+ and SK channel expression in GnRH neurons remains relatively constant across pubertal development. Hence, the expected increase in GnRH neuron cytoplasmic free Ca2+ concentration required for increased GnRH secretion at puberty appears to be due to mechanisms other than altered Ca2+ or SK channel expression, e.g. increased membrane depolarization and subsequent activation of preexisting Ca2+ channels after increased excitatory synaptic input.
This article has been cited by other articles:
 |
|
 |
|
  Z. Chu, J. Andrade, M. A. Shupnik, and S. M. Moenter Differential Regulation of Gonadotropin-Releasing Hormone Neuron Activity and Membrane Properties by Acutely Applied Estradiol: Dependence on Dose and Estrogen Receptor Subtype J. Neurosci., April 29, 2009; 29(17): 5616 - 5627. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 X. Liu, K. Lee, and A. E. Herbison Kisspeptin Excites Gonadotropin-Releasing Hormone Neurons through a Phospholipase C/Calcium-Dependent Pathway Regulating Multiple Ion Channels Endocrinology, September 1, 2008; 149(9): 4605 - 4614. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
X. Liu and A. E. Herbison Small-Conductance Calcium-Activated Potassium Channels Control Excitability and Firing Dynamics in Gonadotropin-Releasing Hormone (GnRH) Neurons Endocrinology, July 1, 2008; 149(7): 3598 - 3604. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. B. Roberts, R. E. Campbell, A. E. Herbison, and K. J. Suter Dendritic Action Potential Initiation in Hypothalamic Gonadotropin-Releasing Hormone Neurons Endocrinology, July 1, 2008; 149(7): 3355 - 3360. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Nishimura, K. Ui-Tei, K. Saigo, H. Ishii, Y. Sakuma, and M. Kato 17{beta}-Estradiol at Physiological Concentrations Augments Ca2+-Activated K+ Currents via Estrogen Receptor {beta} in the Gonadotropin-Releasing Hormone Neuronal Cell Line GT1-7 Endocrinology, February 1, 2008; 149(2): 774 - 782. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
