Abstract
Expression of particular genes in hypothami of ewes was measured across the natural pubertal transition by in situ hybridization. The ewes were allocated to three groups (n = 4); prepubertal, postpubertal and postpubertally gonadectomized (GDX). Prepubertal sheep were euthanized at 20 weeks of age and postpubertal animals at 32 weeks. GDX sheep were also euthanized at 32 weeks, 1 week after surgery. Expression of KISS1, TAC3, PDYN in the arcuate nucleus (ARC), RFRP in the dorsomedial hypothalamus and GNRH1 in the preoptic area was quantified on a cellular basis. KISS1R expression by GNRH1 cells was quantified by double‐label in situ hybridization. Across puberty, detectable KISS1 cell number increased in the caudal ARC and whilst PDYN cell numbers were low, numbers increased in the rostral ARC. TAC3 expression did not change but RFRP expression/cell was reduced across puberty. There was no change across puberty in the number of GNRH1 cells that expressed the kisspeptin receptor (KISS1R). GDX shortly after puberty did not increase expression of any of the genes of interest. We conclude that KISS1 expression in the ARC increases during puberty in ewes and this may be a causative factor in the pubertal activation of the reproductive axis. A reduction in expression of RFRP may be a factor in the onset of puberty, removing negative tone on GNRH1 cells. The lack of changes in expression of genes following GDX suggest that the effects of gonadal hormones may differ in young and mature animals.
Highlights
Puberty is typified by an increase in the secretion of gonadotropin releasing hormone (GnRH) which drives an increase in gonadotropins secretion from the pituitary gland (Clarke& Pompolo, 2005; Ojeda, Roth, et al, 2006), leading to activation of the gonads
One population in the anteroventral periventricular nucleus (AVPV) in rodent or preoptic area (POA) in species such as sheep is involved in the positive feedback action of estrogen that causes the GnRH/luteinizing hormone (LH) surge in females (Hoffman, Le, Franceschini, Caraty, & Advis, 2011; Robertson, Clifton, Iglesia, Steiner, & Kauffman, 2009; Smith, Li, Pereira, & Clarke, 2009; Smith, Popa, Clifton, Hoffman, & Steiner, 2006)
It is generally accepted that kisspeptin signaling is mandatory for puberty (d'Anglemont de Tassigny & Colledge, 2010; Dungan Lemko & Elias, 2012; de Roux et al, 2003; Seminara et al, 2003; Topaloglu et al, 2012), but as to whether an increase in expression of KISS1 or KISS1R is seen at this time across all species is questionable
Summary
Puberty is typified by an increase in the secretion of gonadotropin releasing hormone (GnRH) which drives an increase in gonadotropins secretion from the pituitary gland (Clarke& Pompolo, 2005; Ojeda, Roth, et al, 2006), leading to activation of the gonads. There is a “brake” on the secretion of GnRH and gonadotropins prior to puberty that is not due to feedback effects of steroids from the gonads (Plant, 2015; Plant & Shahab, 2002). Kisspeptin neurons in caudal ARC initiate the positive feedback effect of estrogen on GnRH secretion (Estrada, Clay, Pompolo, Smith, & Clarke, 2006; Smith, 2008; Smith et al, 2009), which is potentiated by activation of the preoptic kisspeptin neurons at the time of the surge (Hoffman et al, 2011)
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