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Biomedical subjects

Tony M Plant

Publications and source records attributed to Tony M Plant.

4 recordsLinked to original sources
PubMed2003

Inhibitory and stimulatory regulation of testicular inhibin B secretion by luteinizing hormone and follicle-stimulating hormone, respectively, in the rhesus monkey (Macaca mulatta).

This study examined the relative role of FSH and LH in governing testicular inhibin B secretion in the rhesus monkey. Adult male monkeys, rendered hypogonadotropic and hypogonadal by administration of a GnRH receptor antagonist (acyline), were implanted with testosterone (T)-filled or empty capsules. Following T-induced restoration of spermatogenesis, both groups received recombinant human FSH and vehicle for 12 d. Juvenile male monkeys received an 11-d infusion of single-chain recombinant human LH and recombinant human FSH, either alone or in combination. In adults, chronic hypogonadotropism resulted in a modest reduction of circulating inhibin B levels, which was more than fully reversed by FSH. In the presence of T, which exerted a marked suppression in inhibin B secretion, FSH restored inhibin B levels only to those observed before acyline treatment. In juveniles, treatment with single-chain recombinant human LH led to a suppression of inhibin B secretion and curtailed the FSH-induced stimulation of this testicular hormone. The T-induced decrease in inhibin B secretion was associated with suppression in inhibin-beta(B) mRNA levels, but FSH stimulation of inhibin B secretion occurred in the absence of clear changes in expression of this subunit gene. These findings indicate that inhibin B secretion by the monkey testis is governed by the inhibitory and stimulatory action of LH and FSH, respectively. The action of LH is presumably indirect and likely mediated by T inhibition of inhibin-beta(B) gene expression. The molecular basis of the stimulatory action of FSH on inhibin B secretion requires further study.

Age Factors↗
PubMed2002

Neuroendocrine mechanisms that delay and initiate puberty in higher primates.

This paper highlights a series of studies using the male rhesus monkey that has led to a model for the control of the onset of puberty in higher primates. The model proposes that the timing of puberty in these species is governed by the duration of a central brake that, during juvenile development, holds in check the hypothalamic network of gonadotropin-releasing hormone (GnRH) neurons, which, in the adult, drive the pituitary-gonadal axis. The neurobiology of this hypothalamic brake, and the physiological mechanisms that time its application and removal, are incompletely understood. Nevertheless, the pubertal resurgence of pulsatile GnRH release, which terminates the juvenile phase of primate development and triggers the initiation of puberty in man and monkeys, is associated with structural and molecular remodeling of the hypothalamus. A major component of this developmental plasticity appears to involve neuropeptide Y (NPY). NPY inhibits GnRH release, and NPY gene expression in the hypothalamus is elevated during juvenile development when GnRH release is restrained. Since the changes in hypothalamic function and morphology that trigger primate puberty unfold in the absence of gonadal steroid feedback, the possibility is raised that, in addition to activating the pituitary-gonadal axis at this stage of development, they may also contribute directly to the causation of behaviors and affective states that emerge at adolescence.

Animals↗
PubMed2002

Leptin and pubertal development.

Sexual development after birth in rodents, nonhuman primates, and humans is driven by the gonadotropin-releasing hormone (GnRH) pulse generator. During the neonatal period in primates, pulsatile GnRH discharge from the medial basal hypothalamus drives an active period of pituitary gonadotropin and gonadal hormone secretion. During the transition from the neonatal to the juvenile period, however, the activity of the GnRH pulse generator is restrained or arrested and gonadotropin and gonadal hormone secretion enters a quiescent period that continues until the onset of puberty. As puberty approaches the GnRH pulse generator is reactivated, resulting in enhanced gonadotropin secretion, accelerated growth, maturation of the gonads, and the achievement of sexual competence. Rodents do not appear to exhibit a developmental phase analogous to the quiescent juvenile period in primates when the GnRH pulse generator is held in check. Instead, progressive maturational changes in the pattern of GnRH pulsatility appear to drive sexual development in rodents. The role that leptin plays in sexual development has not been fully defined, but the balance of current evidence appears to support the idea that, in both rodents and primates, leptin plays a permissive rather than a causal role in timing this process. When body energy reserves rise above a critical level, blood leptin increases to a threshold concentration signaling to the central nervous system that the body can support sexual function. Puberty can apparently occur over a wide range of concentrations above this critical leptin threshold. Leptin does not appear to act as a trigger to time the initiation of puberty but, instead, once leptin reaches this threshold pubertal development may proceed if, and only if, other critical control mechanisms are operational.

Animals↗