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Elife. 2016 Aug 23;5. pii: e16246. doi: 10.7554/eLife.16246.

High-frequency stimulation-induced peptide release synchronizes arcuate kisspeptin neurons and excites GnRH neurons.

Author information

1
Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, United States.
2
Department of Biochemistry, Howard Hughes Medical Institute, University of Washington, Seattle, United States.
3
Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, United States.

Abstract

Kisspeptin (Kiss1) and neurokinin B (NKB) neurocircuits are essential for pubertal development and fertility. Kisspeptin neurons in the hypothalamic arcuate nucleus (Kiss1(ARH)) co-express Kiss1, NKB, dynorphin and glutamate and are postulated to provide an episodic, excitatory drive to gonadotropin-releasing hormone 1 (GnRH) neurons, the synaptic mechanisms of which are unknown. We characterized the cellular basis for synchronized Kiss1(ARH) neuronal activity using optogenetics, whole-cell electrophysiology, molecular pharmacology and single cell RT-PCR in mice. High-frequency photostimulation of Kiss1(ARH) neurons evoked local release of excitatory (NKB) and inhibitory (dynorphin) neuropeptides, which were found to synchronize the Kiss1(ARH) neuronal firing. The light-evoked synchronous activity caused robust excitation of GnRH neurons by a synaptic mechanism that also involved glutamatergic input to preoptic Kiss1 neurons from Kiss1(ARH) neurons. We propose that Kiss1(ARH) neurons play a dual role of driving episodic secretion of GnRH through the differential release of peptide and amino acid neurotransmitters to coordinate reproductive function.

KEYWORDS:

GnRH; dynorphin; mouse; neurokinin B; neuropeptide; neuroscience; slow EPSP; synchronization

PMID:
27549338
PMCID:
PMC4995096
DOI:
10.7554/eLife.16246
[Indexed for MEDLINE]
Free PMC Article

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