Figure 1.

Modulation by non-peptide neurotransmitters, gasotransmitters, and gliotransmitters of GnRH neuron activity and GnRH secretion controlling fertility in mice. Schematic diagram showing non-peptide neurotransmitters (and their receptors), gasotransmitters, and gliotransmitters that act directly on the cell bodies, dendrites, axons, and/or “dendrons” of GnRH neurons to modulate their action potential firing, [Ca²⁺]_i, and GnRH secretion. Transmitters that excite, inhibit, or both excite and inhibit GnRH neurons are indicated in green, red, or purple, respectively, and are listed along with the brain areas in which they are produced. Transmitters that modulate GnRH neuron activity and/or secretion in immortalized GnRH neurons, rat GnRH neurons, or monkey GnRH neurons but have not yet been reported to modulate GnRH neuron activity or secretion in mice are indicated in italics. GnRH secreted from GnRH neuron axon terminals in the ME into the hypothalamo-hypophyseal circulation binds to GnRH receptors on pituitary gonadotrophs to stimulate the synthesis and secretion of LH and FSH into the general circulation. LH and FSH, which are required for gametogenesis and ovulation, bind to receptors in the gonads to stimulate the synthesis and secretion of E, P, and T, which in turn exert negative or positive feedback effects on GnRH neurons (via KP neurons) and gonadotrophs depending on the sex and estrous cycle stage of the animal. Abbreviations are explained at their first occurrence in the main text.