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J Rabii

Publications and source records attributed to J Rabii.

30 records · Page 2Linked to original sources
PubMed1981

Role of serotonin in the regulation of growth hormone and prolactin secretion in the domestic fowl.

Plasma levels of GH and prolactin were measured by radioimmunoassay in male domestic fowl treated with centrally active agents. p-Chlorophenylalanine (pCPA) did not have an effect on tonic levels of prolactin but led to a significant rise in circulating GH concentrations. The three serotonin receptor antagonists tested, methysergide, SQ-10631 and cyproheptadine, each resulted in a significant reduction in plasma prolactin while markedly increasing plasma GH levels. Administration of 5-hydroxytryptophan led to a rise in plasma prolactin and a drop in plasma GH levels in untreated birds or in animals pretreated with pCPA. The serotonin receptor agonist, quipazine, resulted in a marked increase in plasma prolactin and a marked reduction in plasma GH concentrations in untreated birds. In pCPA-pretreated animals quipazine was no longer effective in altering plasma prolactin levels but still caused a significant drop in circulating levels of GH. These results suggest that in the young male domestic fowl serotonin has a stimulatory role in the regulation of prolactin and an inhibitory role in the regulation of GH secretion.

5-Hydroxytryptophan↗
PubMed1980

Effects of intraventricular infusions of 6-hydroxydopamine (6-OHDA) on pituitary LH release and ovulation in the rabbit.

Repeated infusions of 6-hydroxydopamine (6-OHDA) into the third ventricle of the rabbit brain in dosages shown to depress hypothalamic norepinephrine (NE) by more than 80% failed to block the copulation-induced ovulatory surge of LH release from the adenohypophysis in estrogen-primed, multiparous New Zealand White does. Only when infusion of the neurotoxin produced a basal hypothalamic lesion did it intercept the coital stimulus and prevent LH release. In 5 rabbits the initial infusion of 6-OHDA stimulated an LH surge presumably by activating NE release from noradrenergic nerve endings. The failure of chronic depletion of hypothalamic NE to prevent coitally-induced LH release suggests that the transmitter may normally play only a modulatory role in hypothalamopituitary activation in the reflex ovulator, as has also been proposed for its function in cyclic ovulation in the rat. The results suggest that alternative systems may be brought into play to subserve reproductive mechanisms when hypothalamic NE is chronically depleted.

Animals↗
PubMed1980

Maturation of adrenal stress responsiveness in the rat.

Serum and adrenal corticosterone was measured by competitive protein-binding radioassay in rats subjected to saline injection, ACTH administration or ether fumes. Groups of rats were tested at 5, 7, 9, 11, 13, 15, 20 and 25 days of age and measurement of hormone level was made either before treatment, to obtain basal values, or 15 min after treatment. Furthermore, the time-course of corticosterone release after ether was determined in 9- and 15-day-old rats. Neonatal rats responded to ether exposure, ACTH administration or saline injection with a significant rise in serum and adrenal corticosterone concentration above basal levels as early as 5 days of age. By 9 days of age, response to stress was qualitatively the same as that of the 25-day-old rat. The time course of adrenal responsiveness to ether stress was similar in 9- and 15-day-old rats, both age groups showing significant increases in hormone concentration by 15 min. These results contradict the concept of the 'stress non-responsive period' which was promoted by previous studies based on the fluorometric analysis of corticosterone.

Adrenal Glands↗
PubMed1978

Delta-9-tetrahydrocannabinol inhibition of suckling-induced prolactin release in the lactating rat.

To study effects of delta-9-tetrahydrocannabinol (THC) on the regulation of prolactin (PRL) release, a chronic cannula was placed in the right atrium of postpartum lactating rats. Two or more days later their pups were removed for 6--8 hours. A blood sample was drawn from the mother just prior to reintroducing the pups, for determination of basal levels of plasma PRL. A second sample was drawn following 30 min of continuous suckling. THC (1.25 or 4.0 mg/Kg) or vehicle was then injected intravenously and blood samples obtained 30, 60, 120 min later. Relative to vehicle-injected controls, both doses of THC significantly reduced plasma PRL levels and disrupted all components of maternal behavior. These findings indicate that THC inhibits suckling-induced PRL release in the postpartum rat.

Animals↗
PubMed1977

Modulation of the proestrous surge of luteinizing hormone by electrochemical stimulation of the amygdala and hippocampus in the unanesthetized rat.

The roles played by the amygdala and hippocampus in controlling the release of pituitary luteinizing hormone (LH) were studied in the freely moving rat. Monopolar stainless steel electrodes were implanted into the corticomedial (CM) amygdala, basolateral (BL) amygdala and dorsal hippocampus of female rats. When the animal had recovered from surgery and shown two consecutive 4-day estrous cycles, a chronic atrial cannula was introduced during the afternoon of diestrus II. On the following day (proestrus) electrochemical stimulation (ECS) was applied (20--50 micronA anodal DC 120 sec) bilaterally to the amygdala or hippocampus and blood samples were taken every 90 min from 12.00 to 21.00 h for radioimmunoassay (RIA) of LH. Next day, uterine tubes were examined for ova as evidence of ovulation. ECS of the amygdala exerted two divergent influences on LH release. Stimulation of the BL amygdala at 13.45 h, just before the critical period (14.00--16.00 h), was effective in delaying and reducing the LH surge, whereas ECS of the CM amygdala at 12.00 h resulted in an early synchronization in the timing of the LH curves. All of the rats in both groups ovulated, in contrast to the results of applying ECS to the dorsal hippocampus; there the LH surge and ovulation were completely blocked in 7 out of 9 rats. Thus, in the freely moving rat, the hippocampus can exert a potent inhibitory influence on LH release whereas the amygdala plays a modulatory role in the process.

Amygdala↗
PubMed1976

Responses of plasma "estradiol" and plasma LH to ovariectomy, ovariectomy plus adrenalectomy, and estrogen injection at various ages.

Plasma LH and "estradiol" were measured by radioimmunoassay in female rats 5, 10, 15, 20, 25, 30, 40, and 80 days of age, and the changes in these hormone levels 24 h after ovariectomy, ovariectomy plus adrenalectomy, and estrogen injection were determined. Plasma "estradiol" was high at 5 days of age; it increased further to a peak at 15 days of age, and declined thereafter to the low levels seen in adult rats. At each age, plasma "estradiol" declined about 50% 24 h after ovariectomy, whereas it fell to undetectable levels 24 h after ovariectomy plus adrenalectomy at 20 and 80 days of age. Plasma LH did not increase 24 h following ovariectomy at 5 days of age, but it did at all ages thereafter. The peak increase occurred 24 h after ovariectomy at 15 days of age, and the increment was progressively smaller at older ages. Ovariectomy plus adrenalectomy did not cause a significantly greater increase in plasma LH than ovariectomy alone. Injection of estradiol caused a decrease in plasms LH at all ages except in the animals ovariectomized at 5 days of age. The greatest decrease was seen in animals ovariectomized at 15 days of age, with a progressively smaller negative feedback response as age increased. In addition to providing systematic data on changes in the negative feedback effect of estradiol at various ages, the results indicate that, especially in immature animals, there is a circulating substance which cross-reacts with antibodies to estradiol but which does not appear to be a biologically-active estrogen. It does not come from the ovaries and disappears from the circulation if the adrenals as well as the ovaries are removed.

Adrenal Glands↗
PubMed1975

Effect of methysergide, a blocker of serotonin receptors, on plasma prolactin levels in lactating and ovariectomized rats.

The effect of methysergide (MES, 2.5 mg/100 g body wt), a serotonin antagonist, on prolactin release has been studied in lactating and ovariectomized rats. MES caused significant increases in prolactin release in both animals. Studies in ovariectomized, hypophysectomized rats indicate that this effect is not due to a decrease in the peripheral metabolism of prolactin. In vitro incubations of anterior pituitary fragments with MES failed to demonstrate any increase in prolactin release, suggesting that MES does not act directly on the anterior pituitary. Parachlorophenylalanine (PCPA; 32 mg/100 g body wt) decreased brain serotonin levels in ovariectomized rats 5, 24, and 70 h after its administration, yet did not alter plasma prolactin levels. L-tryptophan (6.3 mg/100 g body wt) given 1 and 1 1/2 h prior to sacrifice increased brain serotonin levels, yet did not affect plasma prolactin levels. Neither PCPA nor L-tryptophan altered MES-induced prolactin release. In lactating rats, suckling caused marked increases in plasma prolactin levels, an effect completely abolished by the administration of MES to the mother rats 3 1/4 h prior to suckling. However, MES-induced prolactin release was not altered by prior treatment with MES, either in lactating or ovariectomized rats. Others have shown that suckling releases prolactin through an excitatory serotonergic mechanism. Therefore, the failure of suckling to release prolactin in MES-pretreated rats suggests that MES can block brain serotonin receptors. However, the ability of methysergide to release prolactin in rats with serotonin receptors presumably blocked, suggests that the serotonin receptor-blocking and the prolactin-releasing actions of MES are not related.

Animals↗