Effects of photoperiod on lactotrophs and on dopaminergic and 5-hydroxytryptaminergic neurones in bull calves

1991 ◽  
Vol 129 (1) ◽  
pp. 141-148 ◽  
Author(s):  
S. A. Zinn ◽  
L. T. Chapin ◽  
K. J. Lookingland ◽  
K. E. Moore ◽  
H. A. Tucker

ABSTRACT This study was conducted to determine whether photoperiod-induced changes in serum concentrations of prolactin in cattle were associated with changes in activity of dopamine or 5-hydroxytryptamine (5-HT) neurones in the infundibulum/pituitary stalk and the secretion rate and number of lactotrophs in the anterior pituitary gland. Sixteen prepubertal bull calves (approximately 8 weeks of age) were divided into two groups. One group of eight was maintained on a photoperiod of 8 h light : 16 h darkness (8L : 16D) and the other group was exposed to 16L : 8D for 4 weeks. At this time calves were injected with a decarboxylase inhibitor (m-hydroxybenzylhydrazine dihydrochloride, NSD 1015) which blocks the conversion of dihydroxyphenylalanine (DOPA) to dopamine and of 5-hydroxytryptophan (5-HTP) to 5-HT. Calves were killed with pentobarbital 15 min later. Accumulations of DOPA and 5-HTP in selected brain regions were used as indices of activity of dopamine and 5-HT neurones respectively. Secretory rate and number of prolactinsecreting lactotrophs were determined by reverse haemolytic plaque assay. Relative to calves exposed to 8L : 16D, exposure to 16L : 8D increased serum concentrations of prolactin by eightfold, anterior pituitary gland weight by 23%, release of prolactin from pituitary explants by 57% and the area of the plaque for prolactin-secreting lactotrophs by 70%. There was no difference in the rates of accumulation of DOPA and 5-HTP in the infundibulum/pituitary stalk of animals exposed to 4 weeks of 16L : 8D or 8L : 16D. It was concluded that increased serum concentrations of prolactin in bulls exposed to a photoperiod of 16L : 8D for 4 weeks were associated with increased secretion of prolactin from lactotrophs which was not the result of a coincident reduction in activity of dopamine neurones or an activation of 5-HT neurones that terminate in the infundibulum/pituitary stalk. Journal of Endocrinology (1991) 129, 141–148

1981 ◽  
Vol 88 (2) ◽  
pp. 301-308 ◽  
Author(s):  
ALISON SPEIGHT ◽  
RACHEL POPKIN ◽  
A. G. WATTS ◽  
G. FINK

We have investigated the mechanism by which oestradiol-17β augments pituitary responsiveness to luteinizing hormone releasing factor (LH-RF). Adult rats were ovariectomized on the morning of dioestrus and implanted with either an empty silicone elastomer capsule or a capsule containing oestradiol-17β. Twelve hours later the LH response, tested by injecting 50 ng LH-RF/100 g i.v., was significantly greater in animals implanted with an oestradiol capsule compared with that in animals implanted with an empty capsule. The effect of oestradiol was blocked by sodium pentobarbitone administered 4 h before the test, and this block was overcome by infusing LH-RF during the 4 h period at doses which by themselves were not sufficient to evoke a large release of LH. We also measured LH-RF in pituitary stalk blood collected under Althesin anaesthesia between 4–6 and 12–13 h after ovariectomy and capsule implantation. The concentration of LH-RF in stalk plasma fell between these two collection periods in animals implanted with empty but not with oestradiol-filled capsules. The concentrations of LH-RF in stalk plasma, although relatively low, were significantly higher in animals bearing an oestradiol-containing capsule than the concentrations in peripheral plasma from similarly treated animals, and, by comparison with the LH-RF concentrations in peripheral plasma from animals infused with LH-RF, were sufficiently high to increase significantly the responsiveness of the pituitary gland. These data show that as well as acting directly on the pituitary gonadotrophs, oestradiol-17β increases the responsiveness of the anterior pituitary gland by a mechanism that involves the release and the priming effect of LH-RF.


1968 ◽  
Vol 243 (15) ◽  
pp. 4143-4150 ◽  
Author(s):  
J K McDonald ◽  
F H Leibach ◽  
R E Grindeland ◽  
S Ellis

1979 ◽  
Vol 16 (2) ◽  
pp. 99-112 ◽  
Author(s):  
Thérèse Di Paolo ◽  
Réjean Carmichael ◽  
Fernand Labrie ◽  
Jean-Pierre Raynaud

1984 ◽  
Vol 100 (2) ◽  
pp. 219-226 ◽  
Author(s):  
S. A. Nicholson ◽  
T. E. Adrian ◽  
B. Gillham ◽  
M. T. Jones ◽  
S. R. Bloom

ABSTRACT The effect of six hypothalamic peptides on the basal release of ACTH and that induced by arginine vasopressin (AVP) or by ovine corticotrophin releasing factor (oCRF) from fragments of the rat anterior pituitary gland incubated in vitro was investigated. Dose–response curves to AVP and to oCRF were obtained, and the response to a low dose of oCRF was potentiated by a low dose of AVP. Basal release of ACTH was not affected by any of the peptides in concentrations in the range 10−12 to 10−6 mol/l, and only substance P (SP) and somatostatin (SRIF) inhibited significantly the response to oCRF in a dose-related manner. The responses to a range of doses of oCRF or AVP were reduced by 10−8 and 10 − 6 mol SP or SRIF/1, and to a greater extent by the higher dose. Except in the case of 10−6 mol SRIF/1 on the response to AVP, the response was not further diminished by preincubation of the tissue with the peptide before the stimulating agent was added. The inhibition of the responses to AVP or oCRF by 10−9 mol SP/1 was not potentiated by its combination with either 5 × 10−10 or 10−8 mol SRIF/1; the inhibitory effects were merely additive. The results suggest that although SRIF and SP are able to modulate the release of ACTH from the anterior pituitary gland, they do so only at a high concentration. In the case of SRIF these concentrations are several orders of magnitude higher than those reported to be present in the hypophysial portal blood and therefore a physiological role for this peptide in the control of ACTH secretion is unlikely. J. Endocr. (1984) 100, 219–226


1977 ◽  
Vol 72 (3) ◽  
pp. 301-311 ◽  
Author(s):  
A. E. PANERAI ◽  
IRIT GIL-AD ◽  
DANIELA COCCHI ◽  
V. LOCATELLI ◽  
G. L. ROSSI ◽  
...  

SUMMARY To determine how the sensitivity of the ectopic anterior pituitary gland to the GH-releasing effect of thyrotrophin releasing hormone (TRH) might be affected by the time lapse from transplantation, TRH (0·15 and 0·6 μg) was injected i.v. into hypophysectomized (hypox)-transplanted rats under urethane anaesthesia 1,3, 8,15, 30 and 60 days after transplantation, and plasma samples were taken 5 and 10 min later. Baseline GH values gradually decreased with time from about 16·0 ng/ml (1 day) to about 3·0 ng/ml (30 and 60 days). The TRH-induced GH release was absent 1 day after transplantation, present only with the higher TRH dose 3 and 8 days after transplantation, and clearly elicitable, also with the lower TRH dose (0·15 μg), from 15 up to 60 days. Determination of plasma prolactin concentrations showed a decline from about 85·0 ng/ml (1 day) to about 32·0 ng/ml (8 days); subsequently (15–60 days) prolactin values stabilized. Plasma prolactin levels increased 15 and 60 days after transplantation only when a dose of 0·6 μg TRH was given. In intact weight-matched rats, TRH induced a GH response only at the dose of 1·2 μg while a short-lived but clear-cut prolactin response could be obtained even with the 0·3 μg dose. The present results indicate that: (1) disconnexion between the central nervous system and the anterior pituitary gland greatly enhances GH responsiveness while blunting prolactin responsiveness to TRH; (2) the sensitivity of the anterior pituitary gland to the GH-releasing effect of TRH increases with time from transplantation; (3) TRH is a more effective prolactin-than GH-releaser on the pituitary gland in situ.


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