Neil P. Evans

Bio: Neil P. Evans is an academic researcher from University of Glasgow. The author has contributed to research in topics: Gonadotropin-releasing hormone & Luteinizing hormone. The author has an hindex of 39, co-authored 113 publications receiving 4557 citations. Previous affiliations of Neil P. Evans include West Virginia University & University of Liverpool.

Seasonal changes in gonadotropin-releasing hormone secretion in the ewe: alteration in response to the negative feedback action of estradiol.

Abstract: Two experiments were performed to test the hypothesis that there is a seasonal change in the negative feedback effect of estradiol on episodic secretion of GnRH in the ewe. The first experiment identified a specific estradiol treatment (delivered by s.c. Silastic implant) that produced a 50% decrease in the frequency of pulsatile secretion of LH in ovariectomized ewes during the anestrous season. In the second experiment, this estradiol treatment was administered to ovariectomized ewes during the mid-breeding and anestrous seasons. Separate groups of ovariectomized ewes not treated with estradiol were included during each season to test for a seasonal difference in the effect of estradiol on episodic GnRH and LH secretion. Samples of hypophyseal portal blood (for GnRH) and jugular blood (for LH) were obtained at 5-min intervals approximately one month after placement of the estradiol implants. During the breeding season, no effect of estradiol was observed on either the frequency or size of GnRH and LH pulses. During anestrus, however, estradiol produced a profound suppression of the frequency of GnRH and LH pulses, and an increase in GnRH pulse size. No significant seasonal change was observed in the characteristics of GnRH and LH pulses in ovariectomized ewes in the absence of estradiol treatment. These findings lead to the conclusion that there is a marked seasonal change in the negative feedback effect of estradiol on episodic GnRH secretion in the ewe, with the steroid being maximally effective during anestrus.

Postnatal Stress in Birds: A Novel Model of Glucocorticoid Programming of the Hypothalamic-Pituitary-Adrenal Axis

Abstract: There is growing international interest in how environmental conditions experienced during development can shape adult phenotypes and the extent to which such induced changes are adaptive. One physiological system that links an individual to changes in environmental circumstances during development is the hypothalamic-pituitary-adrenal axis. Mammalian studies have linked early postnatal stress to later changes in the hypothalamic-pituitary-adrenal axis; however, the physiological link [lactational corticosterone (CORT) transfer] between mother and offspring during postnatal development constrains the ability to determine the direct effects of such stressors on subsequent physiology and behavior. Here we present a novel model using an avian species, the zebra finch (Taeniopygia guttata), in which maternal hormonal transfer during postnatal development is likely to be absent. Postnatal exposure of chicks to the stress hormone CORT was manipulated for a 16-d period up until nutritional independence (28 d), and the long-term effects on the physiological response to stress determined. CORT doses were scaled to mimic the physiological response of juvenile birds to a capture-handling-restraint protocol. CORT-fed birds showed exaggerated and prolonged responses to acute stress at 60 d of age. Our results clearly demonstrate that postnatal stress has significant long-term effects on the physiological stress response in birds and provides a potential mechanism underlying long-term behavioural responses to developmental conditions. This study represents the first direct evidence for postnatal glucocorticoid programming of the stress response using this novel model for postnatal stress. This model therefore provides an important tool with which to investigate the role of glucocorticoids in shaping adult phenotypes.

Gonadotropin-releasing hormone requirements for ovulation.

Abstract: This article addresses the role of GnRH in ovulation in the context of two general models of GnRH action-deterministic and permissive. According to the deterministic model, increased GnRH secretion is required to induce the preovulatory LH surge and thus ovulation. The permissive model, in contrast, holds that GnRH secretion need not increase. Rather, the preovulatory LH surge results from enhanced sensitivity of the pituitary gland to GnRH. Studies in rodents and rabbits support the deterministic model whereas evidence in primates suggests that GnRH is permissive. Three lines of evidence are presented to support the conclusion that GnRH plays a deterministic role in sheep. First, a large GnRH surge is secreted together with the preovulatory LH surge. Second, the follicular phase increase in circulating estradiol concentration stimulates this GnRH surge by a positive feedback effect. Third, initiation of the LH surge requires an abrupt increase in GnRH, and maintenance of the LH surge requires continued GnRH support. Collectively, these observations document the fundamental importance of a GnRH surge to ovulation and generation of the estrous cycle of sheep.

Endocrine-Disrupting Chemicals: An Endocrine Society Scientific Statement

Abstract: Thereisgrowinginterestinthepossiblehealththreatposedbyendocrine-disruptingchemicals (EDCs), which are substances in our environment, food, and consumer products that interfere with hormone biosynthesis, metabolism, or action resulting in a deviation from normal homeostatic control or reproduction. In this first Scientific Statement of The Endocrine Society, we present the evidence that endocrine disruptors have effects on male and female reproduction, breast development and cancer, prostate cancer, neuroendocrinology, thyroid, metabolism and obesity, and cardiovascular endocrinology. Results from animal models, human clinical observations, and epidemiological studies converge to implicate EDCs as a significant concern to public health. The mechanisms of EDCs involve divergent pathways including (but not limited to) estrogenic, antiandrogenic, thyroid, peroxisome proliferator-activated receptor , retinoid, and actions through other nuclear receptors; steroidogenic enzymes; neurotransmitter receptors and systems; and many other pathways that are highly conserved in wildlife and humans, and which can be modeled in laboratory in vitro and in vivo models. Furthermore, EDCs represent a broad class of molecules such as organochlorinated pesticides and industrial chemicals, plastics and plasticizers, fuels, and many other chemicals that are present in the environment or are in widespread use. We make a number of recommendations to increase understanding of effects of EDCs, including enhancing increased basic and clinical research, invoking the precautionary principle, and advocating involvement of individual and scientific society stakeholders in communicating and implementing changes in public policy and awareness. (Endocrine Reviews 30: 293–342, 2009)

The GPR54 gene as a regulator of puberty

Abstract: Background Puberty, a complex biologic process involving sexual development, accelerated linear growth, and adrenal maturation, is initiated when gonadotropin-releasing hormone begins to be secreted by the hypothalamus. We conducted studies in humans and mice to identify the genetic factors that determine the onset of puberty. Methods We used complementary genetic approaches in humans and in mice. A consanguineous family with members who lacked pubertal development (idiopathic hypogonadotropic hypogonadism) was examined for mutations in a candidate gene, GPR54, which encodes a G protein–coupled receptor. Functional differences between wild-type and mutant GPR54 were examined in vitro. In parallel, a Gpr54-deficient mouse model was created and phenotyped. Responsiveness to exogenous gonadotropin-releasing hormone was assessed in both the humans and the mice. Results Affected patients in the index pedigree were homozygous for an L148S mutation in GPR54, and an unrelated proband with idiopathic hypogonadotro...