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Calcium and Small-Conductance Calcium-Activated Potassium Channels in Gonadotropin-Releasing Hormone Neurons before, during, and after Puberty

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.

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