Journal
NEUROENDOCRINOLOGY
Volume 102, Issue 3, Pages 184-193Publisher
KARGER
DOI: 10.1159/000370311
Keywords
Canonical transient receptor potential channels; Gonadotropin-releasing hormone; Kisspeptin; T-type calcium current; Hyperpolarization-activated; cyclic nucleotide-gated current; Persistent sodium current
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Funding
- NIDDK NIH HHS [R01 DK068098, DK 68098] Funding Source: Medline
- NINDS NIH HHS [R01 NS043330, R56 NS038809, NS 43330, NS 38809, R01 NS038809] Funding Source: Medline
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Kisspeptin is a neuropeptide that signals via a Gaq-coupled receptor, GPR54, in gonadotropin-releasing hormone (GnRH) neurons and is essential for pubertal maturation and fertility. Kisspeptin depolarizes and excites GnRH neurons primarily through the activation of canonical transient receptor potential (TRPC) channels and the inhibition of K+ channels. The gonadal steroid 1 7 beta-estradiol (E-2) upregulates not only kisspeptin (Kiss1) mRNA but also increases the excitability of the rostral forebrain Kiss1 neurons. In addition, a primary postsynaptic action of E-2 on GnRH neurons is to upregulate the expression of channel transcripts that orchestrate the downstream signaling of kisspeptin in GnRH neurons. These include not only TRPC4 channels but also low-voltage-activated T-type calcium channels and high-voltage-activated L-, N- and R-type calcium channel transcripts. Moreover, E2 has direct membrane-initiated actions to alter the excitability of GnRH neurons by enhancing ATP-sensitive potassium channel activity, which is critical for maintaining GnRH neurons in a hyperpolarized state for the recruitment of T-type calcium channels that are important for burst firing. Therefore, E-2 modulates the excitability of GnRH neurons as well as of Kiss1 neurons by altering the expression and/or function of ion channels; moreover, kisspeptin provides critical excitatory input to GnRH neurons to facilitate burst firing activity and peptide release. (C) 2015 S. Karger AG, Basel
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