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R R Gala

Publications and source records attributed to R R Gala.

At least 109 records · Page 6Linked to original sources
PubMed1976

Further studies on the effects of adrenergic, serotonergic and cholinergic drugs on the afternoon surge of plasma prolactin in ovariectomized, estrogen-treated rats.

The involvement of adrenergic, serotonergic and cholinergic mechanisms in the diurnal surge of plasma prolactin (Prl) secretion has been examined using ovariectomized, polyestradiol phosphate-treated (PEP) rats bearing aortic catheters. An afternoon surge in plasma Prl was observed to peak at 15.00 h and 17.00 h followed by declining levels at 19.00 and 21.00 h. This pattern was observed between 5 and 21 days after PEP administration. The alpha-adrenergic blocker, phenoxybenzamine (Phenox), completely prevented the Prl surge. The beta-blocker, propranolol (Propra), appeared to delay the onset and intensity of the diurnal Prl surge so that maximum levels were observed at 19.00 and 21.00 h. The serotonergic blocker, methysergide (MES), delayed the maximum diurnal Prl level until 21.00 h, while cyproheptadine (Cypro), another serotonergic blocker, significantly inhibited the surge. The muscarinic cholinergic agonist, arecoline (Arec), when administered at 12.00 h, delayed the surge, while the repeated administration of Arec completely blocked the surge. Atropine (Atro) (10 m/kg at 12.00 h and 5 mg/kg every 2 h thereafter) did not have any effect on the Prl surge, but when administered simultaneously with Arec, prevented the inhibitory effect of Arec on Prl release. The data suggested that the adrenergic and serotonergic systems have a positive input in the occurrence and magnitude of the surge and that the cholinergic system does not appear to have a physiologic role in tonically inhibiting Prl release, but may function under certain special conditions.

Animals↗
PubMed1976

Influence of cholinergic receptor blockade on drug-induced prolactin release in the monkey.

The influence of varying doses of perphenazine, thyrotropin-releasing hormone (TRH) and serotonin on prolactin release was examined in two species of monkeys: rhesus (Macaca mulatta) and crab-eating (Macaca fascicularis). The intravenous administration of 0.33 mg/kg body weight of perphenazine or 1.0 mug/kg body weight of TRH gave a greater release of prolactin than higher doses of perphenazine (1.0 mg/kg) or TRH) (3.4 mug/kg), respectively. Prolactin release induced by serotonin at doses of 1, 5 and 10 mug/kg was similar. Both atropine sulfate (Atr-SO4) and atropine methyl nitrate (Atr-MN) at a similar base level potentiated the prolactin releasing action of the high dose of perphenazine suggesting that high doses of perphenazine activate a cholinergic inhibitory component present in the pituitary. Atropine sulfate had no potentiating action on the TRH-induced prolactin release, while Atr-MN appeared to prolong the response of TRH without potentiating it. Neither form of atropine had any influence on serotonin-induced prolactin release. The data indicated that the lower prolactin response to high doses of perphenazine and TRH were brought about by different mechanisms, and that the mechanism for perphenazine appeared to be mediated through a pituitary cholinergic system.

Animals↗
PubMed1976

The interaction of dopaminergic and serotonergic drugs on plasma prolactin in ovariectomized, estrogen-treated rats.

Pharmacologic agents that either block or stimulate dopaminergic or block serotonergic receptors were administered intraarterially alone or in combination to ovariectomized, estrogen-treated rats. Prolactin was estimated by radioimmunoassay of plasma collected by serial blood sampling from chronic aortic catheters. Apomorphine (10 mg/kg) depressed, whereas Pimozide (50 and 250 mug/kg) and Methiothepin (50, 500 and 5000 mug/kg) markedly increased prolactin levels. Apomorphine completely blocked the increases induced by the lowest does of Pimozide and Methiothepin, as well as the initial increases at the higher doses. However, at later time intervals after large doses of Pimozide and Methiothepin in apomorphine-pretreated rats there was a marked rebound of prolactin which was greater than the level induced by each drug alone. The serotonin antagonists SQ 10,631 and methysergide reduced the Pimozide-induced elevation in prolactin levels, suggesting that part of the increase in prolactin following dopaminergic blockage may result from the action of a tonically stimulatory serotonin system that is normally masked by the intense tonic inhibition by the dopaminergic system.

Animals↗
PubMed1976

The influence of cholinergic, adrenergic, and serotonergic drugs on the afternoon surge of plasma prolactin in ovariectomized, estrogen-treated rats.

The effects of systemic administration of cholinergic, adrenergic, and serotonergic drugs on the afternoon surge of plasma prolactin was investigated using ovariectomized, polyestradiol phosphate (PEP)-injected rats bearing aortic catheters. Basal prolactin levels were elevated and similar after PEP administration for a period of 5 weeks, and an afternoon surge in plasma prolactin persisted for a period of 3 weeks before the magnitude of the surge diminished. The plasma estradiol levels were significantly higher for the 1100 and 1300 h samples than for the 1500 and 1700 h samples. Cornified vaginal epithelia were predominant in the vaginal smears of all animals throughout the 49-day experimental period. The cholinergic agonists arecoline, nicotine, and carbachol significantly inhibited the afternoon surge of prolactin. The muscarinic antagonist atropine resulted in a partial inhibition of the surge while the nicotinic antagonist mecamylamine did not have any inhibitory effect. The alpha-adrenergic blockers phenoxybenzamine and phentolamine and the beta-blocker propranolol inhibited the prolactin surge, with phenoxybenzamine being most effective. The administration of the serotonergic antagonist methysergide resulted in only a partial blockade of the afternoon prolactin surge. The data suggest that both the adrenergic and serotonergic systems may have a positive input in the afternoon surge of plasma prolactin. It appears that the cholinergic system does not play a significant role in the afternoon surge.

Animals↗
PubMed1975

Failure of insulin hypoglycemia to produce rise in serum prolactin.

Serum prolactin and growth hormone responses to insulin-induced hypoglycemia were measured in 5 normal individuals. While growth hormone rose appropriately in all subjects studied, serum prolactin levels did not significantly change despite the production of symptomatic hypoglycemia during testing. Prolactin response to insulin hypoglycemia is not a useful diagnostic test for prolactin secretion and cannot be used as such for assessment of pituitary reserve.

Blood Glucose↗
PubMed1975

Induction of pseudopregnancy in the rat by electrochemical stimulation of the brain.

Electrochemical stimulation of the neocortex, VMH-arcuate hypothalamus, medial preoptic area, corticomedial amygdala, and dorsal hippocampus was performed under pentobarbital anesthesia to determine the brain regions involved in prolactin release as evidenced by pseudopregnancy. Stimulation occurred on the day of vaginal estrus, followed 4 days later by uterine traumatization. All animals were sacrificed 8 days after brain stimulation. Medial preoptic sitmulation resulted in an 83% incidence of pseudopregnancy while VMH-arcuate stimulation resulted in 43% incidence. Amygdaloid and hippocampal stimulation resulted in a lower incidence of pseudopregnancy (20 and 24%, respectively). Stimulation of the neocortex or sham stimulation of the five brain regions did not induce pseudopregnancy. These data indicate that the MPOA and VMH-arcuate hypothalamus are areas which may facilitate the release of prolactin necessary for the development of pseudopregnancy. The lower incidence of deciduomata formation resulting from electrochemical stimulation on the amygdala and hippocampus suggest that these areas have a minor effect on stimulating the induction of pseudopregnancy.

Amygdala↗
PubMed1975

Blockage of induced pseudopregnancy by electrochemical stimulation of the limbic system.

Pseudopregnancy induced by cervical stimulation was inhibited by acute electrochemical stimulation of the corticomedial amygdala or dorsal hippocampus under sodium pentobarbital anesthesia (40 mg/kg) in adult, cyclic female Sprague-Dawley rats. The degree to which pseudopregnancy was blocked depended on temporal conditions of brain stimulation and sodium pentobarbital administration. Pentobarbital alone had a suppressing effect on the incidence of pseudopregnancy, especially when it preceded cervical stimulation. Limbic stimulation before cervical stimulation had a tendency to potentiate the suppression of pseudopregnancy by pentobarbital. After cervical stimulation, hippocampal stimulation tended to inhibit the development of pseudopregnancy, potentiating the pentobarbital suppression, while amygdala stimulation tended to override the pentobarbital blockage of pseudopregnancy. These findings suggest a negative influence of these two limbic structures and pentobarbital on the secretion of prolactin.

Amygdala↗
PubMed1975

Studies on prolactin in human serum, urine and milk.

Prolactin activity was measured in serum, urine and milk using a specific human prolactin radioimmunoassay (RIA). Serum, urine and milk were parallel with the human prolactin standard in the RIA. There was no correlation between serum prolactin levels and urinary prolactin activity. Dialysis of urine samples resulted in complete loss of human prolactin activity while the addition of human prolactin to the urine resulted in the recovery of over 50% of the hormone after dialysis. Thus it was concluded that prolactin is not present in urine. In additional experiments it was observed that the RIA prolactin activity in urine was significantly correlated with the osmolality of the urine and that Na+ and K+ were contributory elements. On the other hand, prolactin was found in human milk and correlated well with the expected serum levels of this hormone. This latter finding is interesting because prolactin receptors have been shown to exist on the serosal side of the mammary epithelial cells. The presence of prolactin in milk suggests the possibility of other sites of action for this hormone in addition to the cell membrane.

Dialysis↗
PubMed1975

The influence of adrenergic, dopaminergic, cholinergic and serotoninergic drugs on plasma prolactin levels in ovariectomized, estrogen-treated rats.

Levels of plasma prolactin were estimated in ovariectomized, estrogen-treated rats following the systemic administration of several neural blocking and stimulating drugs. Phenoxybenzamine, an alpha-adrenergic blocker, at high doses, increased plasma prolactin. Phenotlamine, another alpha-adrenergic blocker, and propranolol, a beta-adrenergic blocker, also increased prolactin but the responses were small and transient. Clonidine, an alpha-adrenergic stimulating drug, elevated prolactin levels whereas the beta-adrenergic stimulator isoproterenol had no effect. Dopaminergic blockade by pimozide increased levels of prolactin while stimulation of dopamine receptors by apomorphine decreased prolactin release. Atropine (a muscarinic chilinergic blocker), arecoline (a muscarinic stimulator) and nicotine (a nicotinic cholinergic stimulating drug) did not affect basal prolactin levels. Mecamylamine (a nicotinic blocker) produced a small transient elevation in plasma prolactin. Methiothepin, an alleged serotoninergic blocker, markedly increased prolactin secretion, as did serotonin. The data suggested the involvement of several neurotransmitters in the control of basal secretion of prolactin.

Adrenergic alpha-Antagonists↗
PubMed1975

Influence of anaesthetics on basal, perphenazine-induced and thyrotrophin releasing hormone-induced prolactin secretion in ovariectomized, oestrogen-treated rats.

Plasma levels of prolactin were determined, by radioimmunoassay, in ovariectomized, oestrogen-treated rats after administration of ether, sodium pentobarbitone, urethane, chloral hydrate or ketamine. These anaesthetics, when administered alone, induced sustained increases in the plasma level of prolactin (continuous ether inhalation), no change in prolactin secretion (urethane), or depressions in the level of prolactin (sodium pentobarbitone, chloral hydrate and ketamine). These same anaesthetics when given before perphenazine failed to alter the stimulatory effect of this phenothiazide on prolactin secretion. Sodium pentobarbitone did not alter the normal increase in prolactin concentration after intra-arterial administration of synthetic thyrotrophin releasing hormone (TRH). These results indicated that anaesthetics do not affect the response of either the central nervous system or the anterior pituitary to perphenazine or TRH although they affect prolactin secretion when administered alone. The site of action of anaesthetics must, therefore, be different from that of perphenazine or perphenazine must be capable of overcoming their influence by direct action on the pituitary.

Anesthetics↗
PubMed1975

The influence of 2 br-alpha-ergocryptine (CB-154) and apomorphine on induced prolactin secretion in the crab eating monkey (Macaca fascicularis).

The influence of apomorphine and 2 Br-alpha-ergocryptine (CB-154) on drug-induced prolactin secretion was examined in an intact and an ovariectomized monkey (Macaca fascicularis). Perphenazine administered iv at one mg/kg BW induced a rapid and marked increase in serum prolactin. Apomorphine at a concentration of 4 mg/kg BW administered prior to perphenazine delayed the perphenazine-induced prolactin rise. The iv administration of CB-154 at either 200 or 2000 mu-g/kg BW completely blocked the perphenazine response. Apomorphine injected before TRH suppressed the induced prolactin increase to this releasing hormone while CB-154, even at the very high dose, only partially blocked the TRH-induced prolactin rise. Serotonin injected iv at the level of 10 mg/kg BW induced a rapid and marked increase in serum prolactin and both apomorphine and CB-154 were able to block this response.

Animals↗
PubMed1975

Serum prolactin levels of rats under continuous estrogen stimulation and 2 Br-alpha-ergocryptine (CB-154) injection.

The ability of 2 Br-alpha-ergocryptine (CB-154) to suppress serum prolactin levels was examined in animals under the influence of continuous estrogen stimulation. A single injection of polyestradiol phosphate (Estradurin) once every 21 days produced a constant elevation of serum prolactin. The simultaneous administration of 1 mg/day of CB-154 to estrogenized animals suppressed serum prolactin levels below that of Estradurin alone but the levels were significantly greater than those of animals receiving CB-154 alone. It was suggested that, while CB-154 prevents the release of prolactin, estrogen stimulates prolactin synthesis despite the block of its release. Ether anesthesia may be capable of partially overriding the block of CB-154 and released the stored hormone from the gland.

Animals↗