Monosodium glutamate: Acute and chronic effects on rhythmic growth hormone and prolactin secretion, and somatostatin in the undisturbed male rat

1981 ◽  
Vol 217 (1) ◽  
pp. 129-142 ◽  
Author(s):  
L. Cass Terry ◽  
Jacques Epelbaum ◽  
Joseph B. Martin
1969 ◽  
Vol 45 (2) ◽  
pp. 183-NP ◽  
Author(s):  
C. S. NICOLL ◽  
J. A. PARSONS ◽  
R. P. FIORINDO ◽  
C. W. NICHOLS

SUMMARY A procedure for estimating rat prolactin and growth hormone (somatotrophin, STH), by measuring the optical density of the electrophoretically isolated and stained hormone bands in polyacrylamide gel columns, is described and evaluated. A simple and inexpensive densitometer is also described. Prolactin levels in adenohypophyses and in medium from pituitary incubates were measured by electrophoresis-densitometry (ED) and by the pigeon crop-sac assay. The two methods showed a high degree of correlation. The validity of the ED method for estimating prolactin levels in adenohypophysial tissue and in incubation medium was demonstrated by comparing the prolactin content of adult male and female and of oestrogen-treated male glands and by experiments in vitro. The female pituitary contained about three times more prolactin than the male and the glands of oestrogen-treated males had levels about the same as those of females. It was also shown that the ED method could be used to demonstrate the inhibitory effects of extract of rat hypothalamic tissue on prolactin secretion in vitro by the rat pituitary. Levels of STH in adult male glands, as measured by this method, were comparable to results obtained by others using immunoassays. Propylthiouracil-induced hypothyroidism depressed the STH and prolactin levels in male rat pituitaries, in agreement with the observations of others. The stainability of the prolactin band in rat adenohypophyses was observed to decrease with time when the glands were stored on dry ice. No such change occurred in the staining characteristics of the STH band. Other aspects of the ED method are discussed, including its precision, efficiency, sensitivity, economy and utility.


1973 ◽  
Vol 58 (2) ◽  
pp. 227-231 ◽  
Author(s):  
H. M. LLOYD ◽  
J. D. MEARES ◽  
JOAN JACOBI

SUMMARY The effects of a single injection of 1 mg diethylstilboestrol dipropionate on pituitary mitotic activity and on secretion of growth hormone and prolactin were investigated in male rats on each of the first 15 days following the single dose and then at intervals for a total period of 63 days. Mitotic activity increased to a maximum on day 4 and then gradually diminished. Serum growth hormone was moderately increased during the 2nd week and serum prolactin showed a gradual rise with a return to normal on day 63. In the pituitary gland, growth hormone concentration diminished until day 28, whereas prolactin rose quickly at first, maintained a raised level and increased further on day 43. During the first 12 days, pituitary weight was significantly correlated with serum growth hormone and prolactin concentration. During days 13–28, serum prolactin, but not growth hormone, was significantly correlated with the pituitary mitotic index.


1987 ◽  
Vol 17 (3) ◽  
pp. 601-607 ◽  
Author(s):  
D. J. Nutt ◽  
P. J. Cowen

SynopsisThe effect of diazepam on brain 5-HT-mediated neuroendocrine responses was studied in healthy male volunteers. An acute dose of diazepam (15 mg) significantly attenuated the prolactin and growth hormone responses to intravenous L-tryptophan. After 3 weeks administration of diazepam (25 mg/d) these responses had returned to normal despite much higher plasma diazepam concentrations, suggesting that tolerance had occurred. A reduction in brain 5-HT function may underlie some of the acute therapeutic actions of benzodiazepines. It is possible that excessive ‘rebound’ 5-HT activity may contribute to the abstinence syndrome seen on benzodiazepine withdrawal.


1981 ◽  
Vol 59 (11) ◽  
pp. 1139-1145 ◽  
Author(s):  
Patricia N. Prinz ◽  
Michael V. Vitiello ◽  
Timothy A. Roehrs ◽  
Markku Linnoila ◽  
Elliott D. Weitzman

The acute and chronic effects of phenobarbital and phenobarbital withdrawal on sleep patterns and on plasma growth hormone (GH) and Cortisol fluctuations occurring during sleep were studied. Before bed, five healthy men, aged 21 to 25, were given a placebo on three baseline nights, phenobarbital (100 mg p.o.) for nine nights, and a placebo on a final withdrawal night. Beginning on the third of three consecutive nights in the laboratory, all-night polygraphic sleep recordings and blood samples (obtained every 20 min through indwelling venous cannulae) were collected for the placebo, acute phenobarbital, chronic phenobarbital, and phenobarbital withdrawal conditions.Blood phenobarbital levels ranged between 5 to 9 μg/100 mL across all hours of the chronic drug night. At this low sedative dose, latency to sleep onset and stage 4 sleep were significantly reduced in the chronic drug condition, but REM sleep was not significantly reduced. No significant sleep change was observed on the withdrawal night. Both peak GH level and total integrated GH across the night were unaffected by the acute, chronic, and withdrawal conditions. The pattern of GH release appeared to be altered on the phenobarbital and phenobarbital withdrawal nights as compared with placebo. Nighttime plasma cortisol levels were not significantly altered by any experimental condition.


1978 ◽  
Vol 77 (1) ◽  
pp. 129-136 ◽  
Author(s):  
H. M. LLOYD ◽  
J. M. JACOBI ◽  
J. D. MEARES

Haloperidol, bromocriptine and diethylstilboestrol dipropionate were given in various régimes to male rats to determine their effects on pituitary DNA synthesis, prolactin secretion and growth hormone secretion. Haloperidol increased serum prolactin but did not stimulate pituitary DNA synthesis or reduce pituitary prolactin concentrations. Haloperidol potentiated the effects of oestrogen on serum prolactin and on pituitary DNA synthesis; pituitary prolactin concentrations were greatly reduced, and growth hormone secretion was slightly inhibited. The inhibitory effects of bromocriptine in oestrogen-stimulated rats were demonstrated by smaller pituitary weights and decreased DNA synthesis; serum prolactin levels were lowered and pituitary prolactin concentrations were increased. Haloperidol, given to rats treated with oestrogen and bromocriptine, reversed the inhibitory effects of bromocriptine on DNA synthesis and serum prolactin; pituitary prolactin concentrations fell to well below normal. The results suggest that the haloperidol potentiation of oestrogeninduced pituitary DNA synthesis may depend upon stimulation of prolactin secretion together with reduction of intracellular prolactin levels.


1995 ◽  
Vol 133 (2) ◽  
pp. 189-194 ◽  
Author(s):  
Annamaria Colao ◽  
Bartolomeo Merola ◽  
Diego Ferone ◽  
Paolo Marzullo ◽  
Gaetana Cerbone ◽  
...  

Colao A, Merola B, Ferone D, Marzullo P, Cerbone G, Longobardi S, Di Somma C, Lombardi G. Acute and chronic effects of octreotide on thyroid axis in growth hormone-secreting and clinically non-functioning pituitary adenomas. Eur J Endocrinol 1995;133:189–94. ISSN 0804–4643 The effect of somatostatin on thyroid function was studied in 12 patients with growth hormone (GH)-secreting and eight patients with clinically non-functioning adenomas (NFA) and normal pituitary/ thyroid axis; the patients were subjected to the administration of octreotide (OCT), which is a longacting somatostatin analog. All the patients received an acute test with 100 μg of OCT, both short term (1 month) and long term (6 months), with doses ranging from 300 to 600 μg/day, Serum thyroxine (T4). triiodothyronine (T3), free T4, free T3, thyroglobulin and basal and thyrotropin (TSH)-releasing hormone (TRH)-stimulated TSH were evaluated before and after 1 and 6 months of therapy. Circulating GH and insulin-like growth-factor I (IGF-I) in acromegalics and GH, IGF-I and α-subunit in NFA were assessed at baseline and every month. The acute administration of 100 μg of OCT significantly reduced the TSH response to TRH (p < 0.01) in both acromegalics and NFA. In all the patients OCT administration caused a significant decrease of GH, IGF-I and α-subunit levels (p < 0.01). In addition, after 1 month of therapy both baseline and TRH-induced TSH secretion were decreased significantly in acromegalics and NFA. After 6 months of therapy, baseline and TRH-induced TSH was still reduced in NFA. Conversely, in acromegalics, baseline TSH levels were increased while TSH response to TRH was inhibited. No change of T4, T3, free T4 and free T3 was observed in NFA, whereas a slight but significant increase of T4 and decrease of T3 was recorded in acromegalics. In conclusion, OCT does seem to possess long-term suppressive effects on TSH response to TRH, both in acromegalics and NFA. The lack of basal TSH level inhibition in acromegalics could depend on the restored peripheral conversion of T4 into T3 due to the normalized GH levels during long-term OCT administration. Annamaria Colao, Corso Europa 63, 80127 Napoli, Italy


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