Age-related changes in the response of GH to administration of thyrotrophin releasing hormone (TRH) have been investigated in the domestic fowl. In two strains of chicken the i.v. administration of TRH (10 μg/kg) to 4-week-old male and female birds markedly increased (> 200 ng/ml) the plasma GH concentration within 10 min of treatment and the concentration remained higher than the pretreatment level for at least a further 20 min. Saline (0·9%) administration had no effect on GH secretion in comparable groups of control birds. The same dose of TRH had no effect on plasma GH concentrations in adult (> 24-week-old) laying hens or cockerels. The administration of TRH at doses of 0·1–100 μg/kg (i.v.) or 0·39–50 μg/bird (s.c.) also had very little, if any, effect on GH secretion in laying hens. In laying hens slight increases (10–20 ng/ml, P < 0·05) in the plasma concentrations of GH were observed in one experiment 60 min after the s.c. injection of 100 μg TRH, and in another 60, 90 and 120 min after the serial s.c. injection of TRH (100 μg/bird) every 30 min over a 150 min period. The poor GH response of the adults to TRH stimulation was not due to high circulating concentrations of endogenous gonadal steroids, as surgical gonadectomy had no effect on the GH response to TRH. These results suggest maturational differences in the control of GH secretion in the fowl.
S. HARVEY, R. J. STERLING, and J. G. PHILLIPS
P. J. Sharp, M. C. Macnamee, R. J. Sterling, R. W. Lea, and H. C. Pedersen
The interactions between broody behaviour and changes in concentrations of plasma prolactin and LH were investigated in bantam hens. Adoption of newly hatched chicks caused incubating hens to leave their nests and prevented plasma prolactin decreasing as rapidly as in hens deprived of their nests and not given chicks. Further, the hens allowed to rear chicks came back into lay later (P< 0·001) than the hens not allowed chicks. Plasma prolactin decreased and plasma LH increased in hens deprived of their nests: these changes were reversed when the hens re-nested. The changes in plasma LH and prolactin in nest-deprived and re-nesting birds were not always synchronous; this was particularly clear immediately after nest deprivation when the increase in plasma LH preceded the decrease in the plasma prolactin. Readiness to incubate disappeared between 48 and 72 h after nest deprivation and corresponded with the time when plasma prolactin decreased to baseline values. Administration of ovine prolactin depressed (P<0·01) the initial increase in plasma LH after nest deprivation, but repeated administration of prolactin for up to 72 h failed to suppress plasma LH to the values found in incubating hens. Repeated administration of ovine prolactin at 5- to 8-h intervals for 72 h maintained readiness to incubate in nest-deprived hens. It is concluded that the secretion of prolactin in broody hens is facilitated by the presence of chicks and that increased concentrations of plasma prolactin maintain incubation behaviour. In incubating hens the secretion of LH and prolactin may be partly regulated independently. In addition, LH secretion may also be inhibited by increased plasma prolactin.
J. Endocr. (1988) 118, 279–286
P. J. Sharp, R. J. Sterling, R. T. Talbot, and N. S. Huskisson
The role of chicken vasoactive intestinal polypeptide (cVIP) as a prolactin-releasing factor was investigated in incubating bantam hens. Specific antibodies were raised against cVIP (anti-cVIP) for passive immunization studies, to develop a radioimmunoassay and to localize VIP neurones immunohistochemically in the hypothalamus. The concentration of plasma prolactin decreased after i.v. injection of anti-cVIP: this low concentration being maintained by daily injection of anti-cVIP. Incubating hens injected daily with anti-cVIP deserted their nests after 4·5 ± 0·6 days and returned to lay after 20 ± 1 days. This disruption of incubation behaviour with anti-cVIP was prevented by concomitant, twice daily, injections of 30IU ovine prolactin. The concentration of plasma LH was not immediately affected after injection of anti-cVIP but increased when the hens deserted their nests.
The amount of cVIP, measured by radioimmunoassay, was significantly higher in the median eminence (P < 0·01) and medial basal hypothalamus (P = 0·05) in incubating than in laying hens. No differences were seen in the amounts of cVIP in the preoptic hypothalamus or in a part of the forebrain including the nucleus accumbens, between laying and incubating hens.
Morphological observations were made on immunohistochemically identified cVIP cell bodies in the medial basal hypothalamus. These showed that cVIP cell number, cell area and density of immunoreactive product were significantly (P < 0·05) greater in incubating than in laying hens. Further, the density of cVIP reaction product in the anterior median eminence was also significantly (P < 0·01) greater in incubating than in laying hens.
These observations are consistent with the view that hypothalamic VIP is a physiologically important prolactin-releasing hormone in incubating bantam hens.
Journal of Endocrinology (1989) 122, 5–13
R.J. Sterling, J.M. Gasc, P.J. Sharp, P. Tuohimaa, and E.E. Baulieu
Using a double immunohistochemical technique, LH releasing hormone (LHRH) neurones and 110kDa nuclear progesterone receptor were localized in the hypothalamus of the laying hen. Nuclear progesterone receptor was widely distributed throughout the hypothalamus, occurring in the preoptic, septal, anterior and basal areas. The region where progesterone receptor was revealed in nuclei of neurones overlapped that containing LHRH neurones. However, LHRH cell bodies did not contain progesterone nuclear receptor. It is concluded that the positive feedback action of progesterone on LH release is not mediated by a genomic mechanism within the LHRH neurone.