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At least 55 records · Page 3Linked to original sources
PubMed1988

Effect of metergoline, fenfluramine, and 8-OHDPAT on catalepsy induced by haloperidol or morphine.

The influences of the indirect serotonin agonist fenfluramine (5; 10 mg/kg s.c.), the serotonin antagonist metergoline (5; 10 mg/kg s.c.) and the 5-HT1A agonist 8-OHDPAT (0.1; 0.2; 0.46 mg/kg s.c.) on haloperidol-induced catalepsy in rats or mice and on morphine-induced catalepsy in rats were studied. Morphine-induced catalepsy was enhanced by fenfluramine and attenuated by metergoline, whereas neither fenfluramine nor metergoline had any effect on haloperidol-induced catalepsy. 8-OHDPAT strongly antagonised catalepsy induced by morphine or haloperidol. We conclude that serotonergic transmission plays a major role in effectuating morphine catalepsy but not in effectuating haloperidol catalepsy. The antagonistic effect of 8-OHDPAT suggests a secondary, modulating role for 5-HT1A receptor mediated events in both types of catalepsy.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1978

Effect of metergoline on delayed response in cats and its relation to the metabolism of dopamine and serotonin in neostriatal and mesolimbic neurons.

In cats the effect of Metergoline (Liserdol, Farmitalia) was investigated on the performance of a delayed response task and was related to the associated changes in the concentrations of dopamine, nonadrenaline and serotonin in the brain. Metergoline (14 microgram/kg/day, i.m.) administered during the first 10 days of the training significantly decreased response latencies at delay periods of 0, 3, 9 and 27 sec without significantly affecting the number of errors. Biochemical assays showed that the improved performance correlated with the increased dopamine content of limbic structures and the decreased serotonin content in all brain structures. The concentrations of dopamine in the neostriatum remain unchanged. Response latencies and the number of errors in cats treated with Metergoline were significantly different from those in animals treated with L-DOPA (30 mg/kg/day) probably relfecting the specific biochemical disturbance induced by the two drugs. These results suggest an inhibitory influence of serotoninergic pathways on areas like the meso-limbic system retaining high concentrations of dopamine.

Animals↗
PubMed1975

Effect of metergoline, a powerful and long-acting antiserotoninergic agent, on insulin secretion in normal subjects and in patients with chemical diabetes.

The effect of metergoline on insulin secretion has been evaluated in normal subjects and in patients with chemical diabetes. The repeated administration of metergoline, 2 mg at four-hour intervals to give a total of 24 mg, has enhanced insulin secretion in response to i.v. glucose in normal subjects but not in chemical diabetics. No changes in blood glucose pattern were observed. Under similar conditions, metergoline administration caused a slight but significant decrease in arginine-induced insulin release, both in normal subjects and in chemical diabetics. These results support the concept of a serotoninergic control of insulin secretion and suggest that serotonin exerts different effects on insulin release according to the different stimuli.

Arginine↗
PubMed1982

Metergoline versus bromocriptine in the prevention of puerperal lactation. A double-blind clinical trial.

In a double blind study of the prevention of puerperal lactation, the clinical efficacy of two antiprolactin drugs was compared: metergoline 4 mg tid and bromocriptine 2.5 mg bid were both given for 7 days. An additional 7 days of treatment was administered to 16 patients in whom mammary activity was still present or appeared in the following 3 days. The first 7 day period of treatment was effective in 16/20 women receiving metergoline and in 7/20 on bromocriptine (p less than 0.02); the second period of treatment was effective in all remaining patients. These data indicate that metergoline acts rapidly to arrest puerperal lactation, possibly by a mechanism different from that of bromocriptine.

Bromocriptine↗
PubMed1992

Partial reversal of fluoxetine anorexia by the 5-HT antagonist metergoline.

Experiment 1 showed that the reduction of intake produced by 5 or 10 mg/kg fluoxetine in rats eating either a solid or a liquid meal was partially antagonised by 1 mg/kg of the 5HT1/5HT2 antagonist metergoline but not by 1 mg/kg of the 5HT2 antagonist ketanserin. Experiment 2 examined the meal patterning of rats given 5 mg/kg fluoxetine and 1 mg/kg metergoline. Fluoxetine alone increased the latency to feed, reduced meal size and shifted the inter-pellet interval (IPI) distribution to the right. Metergoline alone had little immediate effect on food intake or other feeding parameters but partially reversed the reduction of food intake produced by fluoxetine. There was a complete reversal of the increased latency to feed and a partial reversal of the depression of meal size. However, the rightward shift of the IPI distribution caused by fluoxetine, which indicated a depression of feeding rate, was more pronounced after combined treatment. We conclude that fluoxetine reduces food intake by enhancing satiety through a serotonergic dependent mechanism but reduces feeding rate through a separate mechanism, whose neurochemical basis remains to be established.

Animals↗
PubMed1995

Effects of d-fenfluramine and metergoline on responding for conditioned reward and the response potentiating effect of nucleus accumbens d-amphetamine.

These studies investigated the effects of the 5-hydroxytryptamine (5-HT) releaser, and re-uptake inhibitor, d-fenfluramine, and the non-selective 5-HT receptor antagonist metergoline, on responding for conditioned reward (CR), and on the potentiation of responding for CR following amphetamine injected into the nucleus accumbens. Water deprived rats were trained to associate a compound stimulus with water delivery during a conditioning phase. During a test phase, water was not delivered but the compound stimulus was delivered according to a random ratio 2 schedule following a response on one of two levers; responding on the other lever was not reinforced. Overall, rats responded at a higher rate on the lever delivering the CR. d-Amphetamine (1, 3 and 10 micrograms) injected into the nucleus accumbens dose-dependently enhanced responding on the CR lever. Treatment with d-fenfluramine (0.5 and 1 mg/kg) reduced responding for the CR, and abolished the potentiating effect of d-amphetamine. Responding on the inactive lever was also reduced by 1 mg/kg but not 0.5 mg/kg d-fenfluramine. The reduction of d-amphetamine's effect on responding for CR was prevented by prior treatment with the 5-HT receptor antagonist metergoline (1 mg/kg). Control experiments showed that changes in thirst and motor performance, as well as deficits in learning ability, cannot account for the effects of d-fenfluramine in this paradigm. In a separate experiment, 1 mg/kg metergoline failed to enhance responding for CR, and to augment the response potentiating effect of a low dose (2 micrograms) of d-amphetamine injected into the nucleus accumbens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Does metergoline selectively attenuate 5-HT mediated prolactin release?

Administration of the non-selective 5-HT receptor antagonist metergoline (0.5 mg/kg) to male rats attenuated the prolactin response to the 5-HT releasing agent d-fenfluramine (7.5 mg/kg) but not to the dopamine receptor antagonist haloperidol (1.5 mg/kg). In contrast, in healthy male volunteers, pretreatment with metergoline (4 mg orally) abolished the prolactin response to intravenous haloperidol (5 micrograms/kg). The findings suggest that in humans blockade of a prolactin response by a conventional oral dose of metergoline cannot be taken as evidence of involvement of 5-HT-mediated mechanisms.

Adolescent↗
PubMedDate not supplied

Effect of metergoline on serum prolactin stimulated by TRH.

The PRL response to TRH was evaluated before and after acute administration of metergoline, an antiserotonin drug, in healthy subjects. The drug was given to two groups of 6 subjects each, at the dose of 4 and 8 mg respectively, either po or by im route. Metergoline significantly inhibited the PRL response to TRH; no significant difference was found between the two doses and the administration routes. Although these findings suggest that the drug may directly inhibit lactotropic cells, an action of metergoline on central nervous system to stimulate PIF or to inhibit PRF release cannot be ruled out, and might as well explain the inhibition of the PRL response to TRH.

Adult↗
PubMed1982

Withdrawal from chronic treatment with metergoline, dl-propranolol and amitriptyline enhances serotonin receptor mediated behaviour in the rat.

Acute treatment of rats with metergoline (2 mg/kg), a serotonin antagonist, prevented the behavioural syndrome produced by the serotonin agonist 5-methoxy-N',N'-dimethyltryptamine (2.5 mg/kg, 5MEODMT). dl-Propranolol (15 mg/kg) and amitriptyline (15 mg/kg) also inhibited the behavioural syndrome. The 5MEODMT behavioural syndrome was attenuated when metergoline or amitriptyline were administered daily for 14 days and 5MEODMT administered 30 min after the injection on day 14. This attenuation was not seen with chronic dl-propranolol treatment. When 5MEODMT was administered 72 h after the last injection of metergoline, amitriptyline or dl-propranolol on day 14, the behavioural syndrome was enhanced. The results suggest that withdrawal from chronic treatment with serotonin antagonists results in functional supersensitivity of serotoninergic neurones.

Amitriptyline↗
PubMed1981

Antagonism of the behavioral effects of 2,5-dimethoxy-4-methylamphetamine (DOM) and quipazine by metergoline.

The present study examined the disruptive effects of the phenethylamine hallucinogen 2,5-dimethoxy-4-methylamphetamine (DOM) and the putative 5-hydroxytryptamine (5-HT) agonist quipazine on fixed ratio-40 (FR-40) operant responding alone or after pretreatment with putative 5-HT antagonist metergoline. Food-deprived male rats were trained to bar press on a FR-40 schedule for food reinforcements; control responding under this schedule is characterized by a rapid, constant rate of responding (approximately 100 response/min). In control animals, both DOM and quipazine produced dose-dependent disruptions of FR-40 performance characterized by periods of non-responding or "pausing". Following pretreatment with 1.0 mg/kg, and to a lesser extent 0.1 mg/kg, metergoline (180 min prior to the session) the dose-response curves for the "pausing" produced by both DOM and quipazine were shifted significantly to the right. Moreover, increasing the dose of DOM about 16-fold and that of quipazine about 8-fold appears to completely override the antagonism by 1 mg/kg metergoline. These results suggest that the "pausing" produced by DOM or quipazine is the result of activation of 5-HT receptors.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗
PubMed1984

Effects of metergoline and quipazine on locomotor activity of rats in novel and familiar environments.

Many studies have investigated the effects on locomotor activity of various manipulations of the brain's serotonin (5-hydroxytryptamine, 5-HT) systems but the results have not been consistent. However, besides employing different techniques for manipulating brain 5-HT, previous studies have differed in size of apparatus, amount of apparatus pre-exposure and length of session. To test the possibility that apparatus familiarity interacts with the effects of 5-HT manipulations on locomotor activity, this variable was manipulated in groups of rats treated with the 5-HT receptor blocker, metergoline or the agonist, quipazine. Within each drug treatment group, 18 rats had prior experience with the activity monitoring photocell chambers (pre-exposed condition) and 18 were not previously exposed (novel condition); each condition was further subdivided into 3 dose subgroups (n = 6). Testing consisted of 3 30-min sessions with subgroups receiving metergoline (0, 2.5, 5.0 mg/kg) or quipazine (0, 2.5, 5.0 mg/kg) 30 min before. Results with metergoline treatment revealed no significant drug effect in the pre-exposed groups but a decrease in activity in the novel condition. Quipazine, on the other hand, had no significant effect in the novel condition but produced a time-dependent effect on activity in the pre-exposed condition. These results suggest that the effects on locomotor activity of compounds affecting 5-HT neurotransmission may interact with the familiarity of the test apparatus and with the duration of testing. Interexperiment differences in these variables may account for some of the inconsistencies previously reported.

Animals↗
PubMed1992

Agonist activity of sumatriptan and metergoline at the human 5-HT1D beta receptor: further evidence for a role of the 5-HT1D receptor in the action of sumatriptan.

We have recently cloned a novel human 5-HT1D receptor subtype termed 5-HT1D beta. CHO K1 cells expressing the human serotonin 5-HT1D beta receptor were assayed to determine the second messenger system of this receptor. Cyclic AMP radioimmunoassays revealed that the 5-HT1D beta receptor is negatively coupled to adenylate cyclase in this cell system. A maximum of 50% inhibition of forskolin stimulated cAMP production was obtained with 5-HT1 receptor agonists which was blocked by the non-selective 5-HT receptor antagonist methiothepin (pKB = 100 nM). The novel anti-migraine drug sumatriptan, a putative 5-HT1D selective compound, acted as an agonist at the 5-HT1D beta receptor. Most notably metergoline, a putative 5-HT1 receptor antagonist, did not block the effects of 5-HT and was found to be acting as a full agonist at the 5-HT1D beta receptor. The ability of metergoline to act as an agonist at the 5-HT1D beta receptor may explain why it does not inhibit 5-HT and sumatriptan induced contraction of dog saphenous vein and other large conducting arteries. These results suggest that the 5-HT1D beta receptor may be the site of action of sumatriptan in preventing migraine, and that metergoline's actions on the dog saphenous vein are not contradictory to that hypothesis, as previously reported.

Cells, Cultured↗
PubMed1982

A study of prolactin, follicle-stimulating hormone, and luteinizing hormone in puerperium: spontaneous variations and the effect of metergoline.

In 80 normal puerperae, serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), including human chorionic gonadotropin (hCG/LH), and prolactin (PRL) levels were evaluated 6 to 29 hours after vaginal delivery. In these puerperae, PRL levels were higher and FSH levels were lower than in menstruating women; hCG/LH levels were very high, due to persisting hCG levels. The values of the three hormones showed a log-normal distribution, and no relationship was found between the three hormones considered in pairs. Thirty-six puerperae chosen from the above 80 were followed during a 5-day period: 24 were not able to breast-feed their babies and were treated with metergoline, an antiserotoninergic agent able to prevent puerperal lactation, 8 or 12 mg/day; 12 additional puerperae, nursing their babies, were evaluated as controls. In lactating women PRL and FSH levels remained steady during the observation period, while hCG/LH levels progressively decreased. Metergoline lowered PRL levels, when employed at both dosages, and FSH levels only at the higher dosage, without affecting the decline of hCG/LH levels. Since dopaminergic drugs are known to lower serum LH levels and not to affect or to increase FSH levels, our data indicate that metergoline might act through a mechanism of action different from dopaminergic drugs.

Adolescent↗
PubMed1998

Effects of serotonin and metergoline on 125[I]-iodocyanopindolol binding parameters to beta-adrenergic receptors in rat brain.

Most ligands which have been employed to investigate the regulation of beta-adrenergic receptors (betaAR) under pathophysiological conditions and in response to pharmacological manipulations have also been shown to have affinity for 5-HT1B receptors. We examined the effects of serotonin and metergoline (10 microM) on 125I-iodocyanopindolol (ICYP, 5-100 pM) binding to betaAR in rat frontal cortex and hippocampus membranes. In both brain regions, the presence of either serotonin or metergoline significantly lowered iodocyanopindolol dissociation constant (Kd) and maximum binding capacity (Bmax). Isoproterenol displacement curves showed that the decrease in receptor density was primarily due to a significant decrease in the receptors in the low-conformational state. Thus, a significant fraction of the apparent ICYP binding to betaAR in the low-conformational state was due to binding to 5-HT1B receptors. Neither serotonin nor metergoline had an effect on the agonist isoproterenol dissociation constant from betaAR in either conformational state.

Animals↗
PubMed1995

Naloxone and metergoline effects on growth hormone response to gamma-hydroxybutyric acid.

Gamma-hydroxybutyric acid (GHB) has been recently used in alcohol detoxification, but conflicting data are available concerning the central mechanism of action of this GABA catabolite. GHB ability to stimulate growth hormone (GH) secretion has been reported. Our previous studies revealed the ability of flumazenil (a benzodiazepine antagonist) to counteract GHB effects on GH secretion. Other hypotheses, including an opioid or serotonergic role of GHB, have been considered. In the present study we investigated GH responses to GHB with or without naloxone (an opiate receptor antagonist) or metergoline (a serotonin receptor antagonist) pretreatment. This study included 10 male healthy volunteers (aged 24.3 +/- 2.9 years) who were submitted to four tests in random order: (A) oral GHB administration; (B) oral GHB and i.v. naloxone administration; (C) oral GHB and oral metergoline administration; and (D) oral placebo and i.v. saline administration. Blood samples for GH assay were collected during the three tests at -15, 0, 15, 30, 45, 60 and 90 min. GHB induced a significant increase in GH plasma levels; naloxone pretreatment did not antagonize GHB action on GH secretion; metergoline significantly decreased GH response to GHB (p < 0.05). No changes were obtained with placebo and saline administration. The opioid system does not seem to be involved in GHB effects on GH-secreting pituitary cells; GHB effects on the serotonergic system influencing GH secretion, on the other hand, cannot be excluded.

Adult↗
PubMed1986

Treatment of hyperprolactinemic amenorrhea with Metergoline.

The ergoline derivative, Metergoline, in a dosage of 4 to 24 mg/day, was administered for one to eight months to 42 patients with hyperprolactinemic amenorrhea. Mean serum prolactin (PRL) concentrations before treatment were 91.2 ng/mL in the patients with functional hyperprolactinemia (N = 29) and 256.9 ng/mL in the patients with pituitary tumor (N = 13). Within four weeks, Metergoline treatment reduced these PRL concentrations to 39.5 ng/mL and 82.9 ng/mL, respectively. In this study Metergoline treatment resulted in restoration of menstruation in a total of 37 patients; 28 patients ovulated, and eight became pregnant. It is considerably more effective in functional hyperprolactinemia than in hyperprolactinemia caused by adenoma.

Adenoma↗
PubMed1978

Metergoline inhibition of thyrotrophin and prolactin secretions in primary hypothyroidism.

The effect of acute oral administration of metergoline on serum thyrotrophin and prolactin levels in six patients with primary hypothyroidism was studied. Metergoline 4 mg by mouth caused a significant decrease in the concentration of serum thyrotrophin and prolactin in all subjects. There was no consistent change in serum thyroxine and triiodothyronine concentrations during the experiment. These findings suggest that metergoline inhibits prolactin and thyrotrophin secretion by a direct action on the hypothalamus or pituitary gland.

Adult↗
PubMed1980

Administration of antisomatostatin serum to rats reverses the inhibition of pulsatile growth hormone secretion produced by injection of metergoline but not yohimbine.

We attempted to determine whether release of endogenous somatostatin (SS) in rats might mediate the apparent inhibition of growth hormone (GH) secretion produced by metergoline of yohimbine injection. Plasma GH levels in adult male rats bearing chronic right-atrial cannulae were measured at 15-min intervals during a 4-hour period around the onset of the daily dark period. Plasma GH levels in control rats (vehicle-injected) rose rapidly from low levels (< 10 ng/ml) just before darkness to very high levels (> 300 ng/ml) around the onset of the dark period, then declined to low values within 2 h. Injection of the serotonin receptor antagonist metergoline (5 mg/kg) or the adrenergic blocker yohimbine (10 mg/kg) 2.25 h before darkness significantly suppressed the subsequent rise in plasma GH levels. The effect of metergoline, but not yohimbine, on plasma GH was markedly reversed when animals were injected intravenously with anti-SS serum (0.5 ml) 1 h after drug administration. These data suggest that circulating SS may mediate the GH inhibition produced by injection of a serotonin receptor blocker; however, other factors are apparently involved in the suppression of GH secretion by yohimbine.

Animals↗