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Submitted on December 18, 2006
Accepted on January 26, 2007
Section of Endocrinology, Department of Pediatrics, University of Chicago, 5841 S. Maryland Ave., MC 5053, Chicago, IL 60637-1470
* To whom correspondence should be addressed. 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 of small-conductance Ca2+-activated K+ (SK) channels, whose activity reflects cytoplasmic free Ca2+ concentration ([Ca2+]i), 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 (GFP) 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+ (IK) channel activator 1-ethyl-2-benzimidazolinone (1-EBIO), were also on average similar in juvenile, pubertal, and adult GnRH neurons. These findings suggest that while 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 [Ca2+]i 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 pre-existing Ca2+ channels following increased excitatory synaptic input.
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