Abstract
Gonadotropin-releasing hormone (GnRH) neuron activity and GnRH secretion are essential for fertility in mammals. Here, I review findings from mouse studies on the direct modulation of GnRH neuron activity and GnRH secretion by non-peptide neurotransmitters (GABA, glutamate, dopamine, serotonin, norepinephrine, epinephrine, histamine, ATP, adenosine, and acetylcholine), gasotransmitters (nitric oxide and carbon monoxide), and gliotransmitters (prostaglandin E2 and possibly GABA, glutamate, and ATP). These neurotransmitters, gasotransmitters, and gliotransmitters have been shown to directly modulate activity and/or GnRH secretion in GnRH neurons in vivo or ex vivo (brain slices), from postnatal through adult mice, or in embryonic or immortalized mouse GnRH neurons. However, except for GABA, nitric oxide, and prostaglandin E2, which appear to be essential for normal GnRH neuron activity, GnRH secretion, and fertility in males and/or females, the biological significance of their direct modulation of GnRH neuron activity and/or GnRH secretion in the central regulation of reproduction remains largely unknown and requires further exploration.
Highlights
Frontiers in EndocrinologyI review findings from mouse studies on the direct modulation of Gonadotropin-releasing hormone (GnRH) neuron activity and GnRH secretion by non-peptide neurotransmitters (GABA, glutamate, dopamine, serotonin, norepinephrine, epinephrine, histamine, Adenosine triphosphate (ATP), adenosine, and acetylcholine), gasotransmitters (nitric oxide and carbon monoxide), and gliotransmitters (prostaglandin E2 and possibly GABA, glutamate, and ATP)
Gonadotropin-releasing hormone (GnRH) neurons, whose cell bodies reside mainly in the preoptic area (POA) of the hypothalamus as well as in the medial septum (MS) and diagonal band of Broca (DBB), provide the final output in the central regulation of mammalian fertility: pulsatile and, in females, surge GnRH secretion from axon terminals in the median eminence (ME)
At their distal dendrons (∼500 μm from the cell body), GnRH neurons appear to be interconnected through dendro-dendritic bundling and associated shared inputs from arcuate nucleus (ARC) KP neurons and possibly other neurons and glial cells, which may provide a mechanism for the synchronization of GnRH neuron activity necessary for pulsatile GnRH secretion, as well as an additional mechanism for its direct modulation [4, 32,33,34,35,36]
Summary
I review findings from mouse studies on the direct modulation of GnRH neuron activity and GnRH secretion by non-peptide neurotransmitters (GABA, glutamate, dopamine, serotonin, norepinephrine, epinephrine, histamine, ATP, adenosine, and acetylcholine), gasotransmitters (nitric oxide and carbon monoxide), and gliotransmitters (prostaglandin E2 and possibly GABA, glutamate, and ATP). Except for GABA, nitric oxide, and prostaglandin E2, which appear to be essential for normal GnRH neuron activity, GnRH secretion, and fertility in males and/or females, the biological significance of their direct modulation of GnRH neuron activity and/or GnRH secretion in the central regulation of reproduction remains largely unknown and requires further exploration
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