• Publications
  • Influence
Increased hypothalamic GPR54 signaling: a potential mechanism for initiation of puberty in primates.
TLDR
Findings are consistent with the hypothesis that GPR54 signaling by its cognate ligand in the primate hypothalamus may be activated at the end of the juvenile phase of development and may contribute to the pubertal resurgence of pulsatile GnRH release, the central drive for puberty.
Preclinical differences of intravascular AAV9 delivery to neurons and glia: a comparative study of adult mice and nonhuman primates.
TLDR
The results indicate that high peripheral tropism, limited neuronal transduction in NHPs, and pre-existing NAbs represent significant barriers to human translation of intravascular AAV9 delivery.
A rapid and simple procedure for chronic cannulation of the rat jugular vein.
TLDR
The present communication describes a cannula that is easy to prepare and a cannulation procedure that is simple and fast for studies on physiologic plasma levels of the pituitary hormones.
An increased intraovarian synthesis of nerve growth factor and its low affinity receptor is a principal component of steroid-induced polycystic ovary in the rat.
TLDR
The results indicate that the hyperactivation of ovarian sympathetic nerves seen in EV-induced PCO is related to an overproduction of NGF and its low affinity receptor in the gland, and suggest that activation of this neurotrophic-neurogenic regulatory loop is a component of the pathological process by which EV induces cyst formation and anovulation in rodents.
Nerve growth factor is required for early follicular development in the mammalian ovary.
TLDR
The results suggest that the delay in follicular growth observed in NGF(-/-) mice may be related to the loss of a proliferative signal provided by NGF to the nonneural endocrine component of the ovary.
Ovarian steroidal response to gonadotropins and beta-adrenergic stimulation is enhanced in polycystic ovary syndrome: role of sympathetic innervation.
TLDR
The results indicate that the increased output of ovarian steroids in PCOS is at least in part due to an enhanced responsiveness of the gland to both catecholaminergic and gonadotropin stimulation, and support the concept that an alteration in the neurogenic control of the ovary contributes to the etiology of PCOS.
Textbook of endocrine physiology
TLDR
Sergio R. Ojeda, James E. Griffin, and Norman M. Kaplan: Organization of the Endocrine System.
Epigenetic Control of Female Puberty
TLDR
This work shows that an epigenetic mechanism of transcriptional repression times the initiation of female puberty in rats and identifies silencers of the Polycomb group (PcG) as principal contributors to this mechanism and shows that PcG proteins repress Kiss1, a puberty-activating gene.
Activation of A-type gamma-aminobutyric acid receptors excites gonadotropin-releasing hormone neurons.
TLDR
In green fluorescent protein-identified adult mouse GnRH neurons in brain slices, gramicidin-perforated-patch-clamp experiments revealed the reversal potential (E(GABA))) for current through GABA(A)Rs was depolarized relative to the resting potential, suggesting the physiological consequence of synaptic activation of GABA (A)R in Gn RH neurons is excitation.
...
...