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Fig. 1. GnRH neuron activity and regulatory factors of ARN kisspeptin neuron-specific ultradian calcium oscillations in neonates. (A) After birth, GnRH neurons in neonates show an early increase in activity. After suppression of the activity during the juvenile period, the GnRH pulse is reactivated in the peripubertal period. In females, the late development of the AVPV kisspeptin neurons in the pubertal period enables generation of the GnRH surge (Herbison, 2016). (B) In neonatal mice, hypothalamic ARN kisspeptin neurons are connected to GnRH neurons that have cell bodies in the preoptic area (POA) and axon terminals in the median eminence. ARN kisspeptin neuronal networks can generate ultradian calcium oscillations that are dependent on voltage-gated sodium (Na+) or potassium (K+) channels and endoplasmic reticulum (ER)-dependent calcium (Ca2+) release or uptake. However, signaling through neurokinin B receptor (NK3R) or dynorphin (Dyn), which are known to auto-regulate ARN kisspeptin neurons, or gap junctions composed of connexins 36, 50, or 43, were marginally effective at the neonatal stage. Furthermore, N-methyl-D-aspartate (NMDA) receptor- and gamma-aminobutyric acid (GABA) type A receptor-mediated neurotransmission were involved in regulating the ultradian calcium oscillations.
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