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At least 253 records · Page 14Linked to original sources
PubMed2002

Serotonin sets the day state in the neurons that control coupling between the optic lobe circadian pacemakers in the cricket Gryllus bimaculatus.

The bilaterally paired optic lobe circadian pacemakers of the cricket Gryllus bimaculatus mutually exchange photic and circadian information to keep their activity synchronized. The information is mediated by a neural pathway, consisting of the so-called medulla bilateral neurons, connecting the medulla areas of the two optic lobes. We investigated the effects of serotonin on the neural activity in this coupling pathway. Spontaneous and light-induced electrical activity of the neurons in the coupling pathway showed daily variations, being more intense during the night than the day. Microinjection of serotonin or a serotonin-receptor agonist, quipazine, into the optic lobe caused a dose- and time-dependent inhibition of spontaneous and light-induced responses, mimicking the day state. The amount of suppression was greater and the recovery from the suppression occurred faster during the night. Application of metergoline, a non-selective serotonin-receptor antagonist, increased spontaneous activity and light-evoked responses during both the day and the night, with higher effect during the day. In addition, metergoline effectively attenuated the effects of serotonin. These facts suggest that in the cricket's optic lobe, serotonin is released during the daytime and sets the day state in the neurons regulating coupling between the bilaterally paired optic lobe circadian pacemakers.

Animals↗
PubMed1986

Participation of opiate and serotonergic systems in brain conditioning stimulatory inhibition of the potentials evoked by tooth pulp stimulation in the pars caudalis of the trigeminal sensory nucleus of the rat.

Effects of conditioning stimulations of the nucleus raphe magnus (NRM), nucleus reticularis paragigantocellularis (NRPG), mesencephalic periaqueductal central gray (PAG), nucleus dorsomedialis hypothalami (DMH), corpus striatum (CP), sensory cortex (SCT) and visual cortex (VCT) and actions of morphine, naloxone and metergoline on the potentials recorded from the pars caudalis of the trigeminal sensory nucleus evoked by the electrical stimulation of rat incisor pulps were examined. The spinal potentials evoked by electrical stimulation of the pulp consisted of 3 components. Component 2 was mainly inhibited by morphine and antagonized by naloxone. Conditioning stimulation of NRM, NRPG, PAG, CP, SCT and DMH strongly inhibited component 2. VCT did not show any inhibition. 33-67% of antagonism was observed by naloxone in the NRM, NRPG, PAG, CP, SCT and DMH. On the other hand, 27-44% of antagonism was observed by metergoline, and the antagonism was not enhanced by the additional administration of naloxone. These results conclusively show that the endorphin system as well as the serotonergic system is in the series involved in the descending inhibition for nociception in the trigeminal sensory nucleus.

Animals↗
PubMed1980

Interaction of dopaminergic and antiserotoninergic drugs in the control of prolactin and LH release in normal women.

Prolactin (Prl) release, both in the experimental animal and in man, is stimulated by serotonin (5HT) and inhibited by dopamine (DA). Data also suggest that LH release in the animal is stimulated by norepinephrine and inhibited by DA. The role of 5HT in the control of LH release is less clear. It would appear to stimulate episodic LH release and to inhibit the LH surge at the pro-oestrus in animals, but the effect of 5HT on LH release has not yet been evaluated in man. In the present paper we have studied the effect of various DA-ergic drugs (DA, iv l-dopa, po l-dopa and bromoergocriptine) and of two anti-5HT drugs, metergoline and methysergide, on Prl and LH release in normal women. DA-ergic drugs lowered plasma Prl and LH levels; anti-5HT drugs, at doses able to lower Prl levels, did not affect basal LH release nor the inhibiting effect of iv l-dopa on LH release. These data indicate that DA inhibits both LH and Prl release in normal women, and that 5HT stimulates Prl release but is not involved in the regulation of LH secretion. The fact that, at variance to all the DA-ergic drugs used, the two anti-5HT drugs did not vary LH release, suggests that metergoline and methysergide are devoid of DA-ergic activity in man, at least at the doses able to inhibit Prl release.

Adult↗
PubMed1987

The behavioural response to the 5-hydroxytryptamine1B (5HT1B) receptor agonist--RU-24969 may exhibit a circadian variation in the mouse.

The effects of the 5-hydroxytryptamine1B receptor agonist RU-24969 on locomotor activity were examined at different times during the light-dark cycle in the mouse. A dose-dependent hyperlocomotion was observed following RU-24969 administration which was partially antagonised by the non-selective 5-hydroxytryptamine receptor antagonist metergoline. The dose ratios for RU-24969 at two different times tested (8 hr after lights-on, L8; 5 hr after lights-off, D5) were significantly different in the presence of metergoline (2 and 5 mg/kg i.p.). The data suggest that the receptor(s) involved in the behavioural response to RU-24969 in the mouse exhibit a circadian variation.

Animals↗
PubMedDate not supplied

Pharmacological characterisation of [35S]-GTPgammaS binding to Chinese hamster ovary cell membranes stably expressing cloned human 5-HT1D receptor subtypes.

[35S]-GTPgammaS binding has been used to study the function of cloned human 5-HT1D receptor subtypes stably expressed in chinese hamster ovary (CHO) cells. 5-HT stimulated [35S]-GTPgammaS binding to membranes from cells expressing 5-HT1Dalpha or 5-HT1Dbeta receptors. In membranes containing 5-HT1Dbeta receptors, 5-CT and sumatriptan stimulated binding to a similar extent as 5-HT while yohimbine, metergoline and 8-OHDPAT were partial agonists. The order of potency for agonists was 5-CT > 5-HT > metergoline > sumatriptan > yohimbine > 8-OHDPAT. The stimulation of binding by 5-HT in membranes containing 5-HT1Dbeta receptors was potently antagonised by methiothepin (pA2 8.9 +/- 0.1). The overall pharmacological profile for the human 5-HT1Dbeta receptor, defined using [35S]-GTPgammaS binding, agreed well with that reported for inhibition of forskolin-stimulated adenylyl cyclase. In addition, methiothepin and ketanserin inhibited basal [35S]-GTPgammaS binding to membranes containing 5-HT1Dalpha or 5-HT1Dbeta receptors, suggesting that these compounds show negative efficacy at 5-HT1D receptor subtypes. The data show that [35S]-GTPgammaS binding is a suitable method for studying the interaction between cloned human 5-HT1D receptors and G-proteins.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1975

[Charge-transfer complexes of indolalkylamine and ergoline derivatives].

Charge-transfer complexes of 1,3,5-trinitrobenzene and pyromellitic dianhydride with indolalkylamines (5-hydroxytryptamine, dimethyltryptamine, etryptamine) and with ergoline derivatives having antiserotonin activity (methysergide, methylergometrine, metergoline, nicotergoline) were studied. The value of the association constant of indole derivatives with trinitrobenzene is influenced by variations on the chain; on the contrary, with pyromellitic dianhydride - only etryptamine and dimethyltryptamine form CT-complexes - the different behaviour can not be correlated with any particular structural characteristics. The association constant values of ergoline derivatives with trinitrobenzene are of the same order of magnitude as that of serotonin; with pyromellitic dianhydride only metergoline and nicotergoline form CT-complexes.

Metergoline↗
PubMed2003

Midbrain raphe modulation of nonphotic circadian clock resetting and 5-HT release in the mammalian suprachiasmatic nucleus.

Serotonin (5-HT) is an important regulator of the mammalian circadian clock of the suprachiasmatic nucleus (SCN); however, critical questions remain concerning the control of serotonergic activity in the SCN and how this relates to the putative clock-resetting actions of 5-HT. Previously, we reported that electrical stimulation of the dorsal raphe nucleus (DRN) or median raphe nucleus (MRN) in hamsters evoked 5-HT release in the SCN. This DRN-stimulated 5-HT release was blocked by systemic injection of 5-HT antagonists, indicating a 5-HT receptor-mediated pathway from the DRN to the SCN. In the present study, targeted injections of the 5-HT1,2,7 antagonist metergoline or the selective 5-HT7 antagonist DR4004 into the DRN or MRN attenuated DRN-electrically stimulated SCN 5-HT release, supporting a multisynaptic DRN-->MRN-->SCN route. Intra-DRN and intra-MRN injections of the GABA(A) antagonist bicuculline significantly stimulated SCN 5-HT release, whereas intra-DRN or intra-MRN injections of the GABAA agonist muscimol suppressed this release. The 5-HT release induced by intra-DRN bicuculline was also blocked by co-injection of DR4004. In complementary behavioral trials, SCN 5-HT release associated with a phase-advancing sleep deprivation stimulus at midday was prevented by intra-DRN injection of metergoline. Also, phase-advance shifts induced by novel wheel access at midday were suppressed, but not blocked, by intra-DRN injection of DR4004 or muscimol. These results indicate that 5-HT7 and GABAergic receptors of the DRN and MRN regulate behaviorally induced 5-HT release in the SCN, and that DRN output modulates nonphotic phase-resetting responses.

Animals↗
PubMed1992

Effects of various serotonin receptor subtype-selective antagonists alone and on m-chlorophenylpiperazine-induced neuroendocrine changes in rats.

Administration of m-chlorophenylpiperazine [m-CPP, a serotonin (5-HT) agonist] to rats increases plasma concentrations of prolactin and corticosterone. Pretreatment with various doses of ritanserin (5-HT1C/5-HT2 antagonist), ICS 205-930 and MDL-72222 (5-HT3 antagonists), iodocyanopindolol or CG361A (beta adrenoceptor antagonists) and spiperone (5-HT1A/5-HT2 antagonist) did not attenuate m-CPP-induced increases in plasma concentrations of prolactin. In contrast, pretreatment with various doses of metergoline (5-HT1/5-HT2 antagonist), propranolol (beta adrenoceptor antagonist that also has binding affinity for 5-HT1A, 5-HT1B and 5-HT1C sites), mesulergine and mianserin (5-HT1C/5-HT2 antagonists) attenuated m-CPP-induced increases in plasma prolactin. On the other hand, m-CPP-induced increases in corticosterone concentrations were attenuated only by pretreatment with a low dose of mianserin and a high dose of spiperone. When administered without m-CPP, metergoline, mesulergine, ritanserin, ICS 205-930 and high doses of mianserin, spiperone and propranolol increased plasma corticosterone secretion. On the other hand, none of the antagonists used in the present study, except spiperone, had any significant effect on plasma prolactin secretion. These findings suggest that m-CPP-induced prolactin secretion is mediated by stimulation of 5-HT1C receptors while corticosterone secretion may be mediated either by an antagonistic effect at 5-HT3 receptor subtype or by nonserotonergic mechanisms. Alternatively, enhancement of corticosterone secretion by the 5-HT antagonists when administered alone may be responsible for their failure to block m-CPP-induced corticosterone secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1979

[Role of the prostaglandin system in the monoaminergic control of prolactin release in the rat].

In ovariectomized rats treated with estradiol benzoate, the pre-treatment with bromocriptine or metergoline on increase of PRL secretion induced by some prostaglandins has been investigated. The PGs used were able to hinder the drop in PRL levels induced by metergoline, a blocker of 5-HT receptors, but not that produced by bromocriptine, a dopamine receptor agonist. Therefore it is possible to suppose that the PGs are involved in the monoaminergic hypothalamic regulation of the PRL secretion.

Animals↗
PubMedDate not supplied

Some behavioral effects of histamine H1-, and H2-receptor agonists in rats.

2-Pyridylethylamine (2-PEA) and 4-methylhistamine (4-MeHI) when given intraventricularly at doses of 30 and 100 microgram had no discernible effect on spontaneous locomotor activity and did not visibly change gross behavior of rats. 4-MeHI(100 micrograms) injected to tranylcypromine-pretreated rats increased locomotor activity and induced head twitches. Locomotor activation was not antagonized by either cimetidine or metergoline but was prevented by alpha-methyl-p-tyrosine and haloperidol and reduced by phentolamine. 4-MeHI-, and histamine (HI)-induced head twitches were not antagonized by either cimetidine or metiamide but were completely abolished by metergoline and p-chlorophenylalanine. It is concluded that 4-MeHI--induced locomotor activation and both HI-, and 4-MeHI-induced head twitches are respectively catecholamine-, and serotonin-dependent phenomena. The behavioral effects of HI and HI H1-and H2-receptor agonists are discussed with regard to possible HI interactions with both catecholamine and serotonin systems in brain.

Animals↗
PubMed1979

[Antiprolactin therapy in the treatment of benign lesions of the breast. Comparison of bromocryptine and methergoline].

The Authors have treated 11 patients with benign breast diseases (fibroadenosis or fibrocystic disease) with two prolactin inhibitor drugs -- metergoline and bromocriptine -- at the dose of 8 mg/die and 7,5 mg/die respectively for sixty days with a 30 days interval from one to the other. All patients, except one, had normal serum prolactin levels before the trial; during the treatment with metergoline no long-term changes in serum prolactin levels were observed; on the contrary, bromocriptine reduced significantly prolactin values for the whole duration of the therapy. Negative clinical results were obtained with the first drug, while bromocriptine allowed to reach an 80% of positive results at the end of the trial. Coming from previous experience, the Authors conclude that the positive therapeutic effect of bromocriptine treatment is connected with the maintenance of prolactin reduction.

Adult↗
PubMed1984

Two novel agents affecting eating through an action on monoaminergic systems.

The pharmacological effects of two newly synthesized anorectic agents CM 57373 (4-amino-1-(6-bromopyrid-2-yl) piperidine hydrochloride) and CM 57493 (4-(3-trifluoromethylphenyl)-1-(2-cyanoethyl)-1,2,3,6 tetrahydrophyridine hydrochloride) have been studied. Both drugs decreased food intake dose dependently in rats deprived of food for 20 h/d. The doses that inhibited food intake by 50 percent (ID50) were 9.74 mg kg-1 p.o. for CM 57493 and 7.37 mg kg-1 p.o. for CM 57373. The general behaviour of the rats was not affected at anorectic doses and no amphetamine-like stimulation was observed. The anorectic effect of CM 57373 was selectively, but not completely, antagonized by metergoline and methysergide, two antagonists of serotoninergic receptors in the central nervous system. Neither noradrenaline antagonists (propranolol and phentolamine) nor a dopamine antagonist (penfluridol) affected the anorexia induced by CM 57373. These results indicate that the anorectic effect of CM 57373 is, at least, partially mediated by the serotoninergic system. The mechanism of action of CM 57493 is more complex, since several distinct neurotransmitter systems appear to be involved in its effect. In cross-tolerance experiments with fenfluramine, there was a reduction of the anorectic activity of CM 57493, suggesting similar mechanisms of action for these two drugs, even though pretreatment with metergoline or methysergide antagonized the anorectic effect of fenfluramine but not that of CM 57493. The anorectic effect of CM 57493 was antagonized by pretreatment with propranolol, a beta-noradrenergic antagonist, suggesting an involvement for the beta-noradrenergic system as well. Pretreatment with phentolamine or penfluridol did not modify the effect of CM 57493 on food intake. In-vitro and in-vivo biochemical studies showed that CM 57373 and CM 57493 act mainly on central serotoninergic mechanisms. CM 57373 is a serotonin releaser and a serotonin reuptake inhibitor. But, unlike fenfluramine which affects the storage pool for 5HT, it releases 5HT mainly from a functional pool. CM 57493 did not affect serotonin release and uptake but exhibited a high affinity to serotonin postsynaptic receptors.

Animals↗
PubMed1984

Differential actions of serotonin antagonists on two behavioral models of serotonin receptor activation in the rat.

Ligand binding studies have identified certain serotonin (5-HT) antagonists with selective affinity for 5-HT2 receptors and other serotonin antagonists with affinity for both 5-HT1 and 5-HT2 receptors. This study compared the actions of ketanserin and pipamperone, selective 5-HT2 receptor antagonists, with metergoline and methysergide, nonselective 5-HT antagonists, on two behavioral responses in rats that are produced by the activation of 5-HT receptors: 1) the head shake response and 2) the 5-HT syndrome. Both the selective and the nonselective 5-HT antagonists blocked the head shake response produced by 5-hydroxy-L-tryptophan. The order of relative potency was: metergoline greater than ketanserin greater than pipamperone greater than methysergide. All four antagonists also blocked the head shake response produced by the 5-HT agonist quipazine. In contrast, the symptoms of the 5-HT syndrome produced by 5-methoxy-N,N-dimethyltryptamine were blocked by pretreatment with the nonselective 5-HT receptor antagonists but not by the 5-HT2 receptor antagonists. The differential actions of 5-HT antagonists on these behavioral responses suggest that different 5-HT receptors are involved in the head shake response and the 5-HT syndrome. That the order of relative potency for these drugs to block the head shake response was the same as their reported affinity for the 5-HT2 receptor suggests that the 5-HT2 receptor is involved in the head shake response. In contrast, the ability of 5-HT antagonists with affinity for the 5-HT1 receptor to block the 5-HT syndrome and the inability of 5-HT2 receptor antagonists to block the syndrome suggests that this behavioral response probably involves the activation of 5-HT1 receptors.

Animals↗
PubMed1984

[Plasma prolactin response to suckling stimulation in puerperal women].

Plasma PRL response to suckling was studied during the 1st week, between the 1st and 2nd weeks and between the 4th and 5th weeks postpartum. During the 1st week, mean (+/-SE) basal PRL significantly rose from 201.9 +/- 27.5 ng/ml to 294.7 +/- 25.6 ng/ml at 15 min and 300.9 +/- 25.9 ng/ml at 30 min after suckling had begun. Between the 1st and 2nd weeks, mean basal levels and the responses to suckling were not significantly different from those during the 1st week. Between the 4th and 5th weeks, mean basal values were considerably lower and the responses to suckling were significantly greater [51.8 +/- 6.9 ng/ml at 0 min; 212.9 +/- 14.8 ng/ml at 15 min and 239.3 +/- 21.4 ng/ml at 30 min] than those within the 2nd week. Assessment of intersubject variations within the 5th week revealed that a significant inverse correlation existed between the basal levels and the suckling-induced maximum increments in PRL (r = -0.538, p less than 0.001). The effects of the oral administration of two serotonin antagonist (cyproheptadine and metergoline) and the dopamine infusion on plasma PRL levels and the response to suckling were investigated during the 1st week postpartum. Metergoline and dopamine suppressed basal PRL levels and abolished the response to suckling, whereas cyproheptadine suppressed the response less effectively without modifying the basal levels. These data suggest that in the early puerperal period an inverse relationship exists between the basal level and the response to suckling in plasma PRL. The suckling-induced PRL release may be mediated via a serotonergic as well as a dopaminergic pathway.

Cyproheptadine↗
PubMed1996

Which type of 5-hydroxytryptamine receptor mediates relaxation of the longitudinal muscle of guinea pig proximal colon in vitro?

Concentration-dependent 5-hydroxytryptamine (5-HT) relaxations of guinea pig proximal colon were evoked in the presence of atropine (0.2 microM). 5-HT effect was neuronally mediated since it was blocked by tetrodotoxin (TTX) (0.5 microM). The type of 5-HT receptor mediating the relaxations was investigated using both 5-HT agonists and antagonists. Selective 5-HT3 antagonists tropisetron (10, 50, 500 nM) and ondansetron (1 microM) shifted the concentration-response curves for 5-HT to the right. Another 5-HT3 antagonist MDL 72222 (0.5 microM), 5-HT1/5-HT2 antagonists methiothepin (0.1 microM) and metergoline (0.1 microM), 5-HT(1A,B) antagonist propranolol (l microM) and 5-HT1B antagonist isamoltane (10 nM) were ineffective. Specific agonist of 5-HT3 receptors 2-methyl-5-hydroxytryptamine (2-methyl-5-HT) and agonist of 5-HT1 receptors 5-carboxamidotryptamine (5-CT) also relaxed the preparation, although the relaxation was not 5-HT relaxation. Neither was it neurogenic because it persisted in the presence of TTX (0.5 microM). The concentration-response curve for 2-methyl-5-HT was not affected by ondansetron (1 microM) or tropisetron (0.5 microM), but it was shifted to the right in the presence of 5-HT1/5-HT2 receptor antagonists methiothepin (0.1 microM) and metergoline (0.1 microM) and in the presence of 5-HT(1Da)/5-HT2A receptor antagonist ketanserin (1 microM). Methiothepin (0.1 microM) also inhibited the relaxations evoked in the presence of 5-CT. Specific agonist of 5-HT4 receptors 5-methoxytryptamine did not exert any effect on the preparation. It is suggested that there are two different mechanisms of relaxation in the guinea pig proximal colon. One is neurogenic and involves the activation of 5-HT3 receptors located on inhibitory neurons to the muscle; the other is myogenic and might be mediated via yet unclassified 5-HT receptors located on the muscle.

Animals↗
PubMed1997

Pharmacology of the serotonergic inhibition of steroid-induced reinitiation of oocyte meiosis in the teleost Fundulus heteroclitus.

Serotonin (5-HT) was found to inhibit steroid (17 alpha,20 beta-dihydroxy-4-pregnen-3-one; 17,20 beta P)-induced resumption of oocyte meiosis (oocyte maturation) in vitro in the teleost Fundulus heteroclitus. Serotonin inhibited both follicle-enclosed and denuded oocytes, which indicates the presence of oocyte-associated 5-HT sensitive sites. The response of oocytes to 5-HT was characterized pharmacologically, i.e., the capacity of serotonergic agonists and antagonists to mimic or block the 5-HT inhibition of the steroid-induced oocyte maturation was assessed by the changes in the percentage of oocyte germinal vesicle breakdown (GVBD). Dose-response curves for each compound were drawn and compared. The rank order of potency among the agonists was: 5-HT > 5-methoxytryptamine > tryptamine = 5,6-diHT = 5-carboxidotryptamine > 5,7-diHT = 5-methoxy-dimethyltryptamine > alpha-methyl-5HT > 2-methyl-5HT. Incubation of ovarian follicles with high doses of some antagonists (mianserin and metergoline) induced oocyte GVBD, although this effect was associated with high levels of oocyte atresia during GVBD or shortly after maturation. Consequently, doses of the antagonist too low to induce GVBD were tested for their ability to block the 5-HT inhibitory action; the rank order of potency was: MDL-72222 = metoclopramide > metergoline > propanolol > ketanserin. Dopamine, acetylcholine, epinephrine, and norepinephrine could also inhibit 17,20 beta P-induced GVBD, although at doses much higher than those of 5-HT; melatonin and histamine had no effect on oocyte maturation. These results suggest that specific receptors mediate the inhibitory action of 5-HT on the steroid-triggered meiosis resumption. The pharmacological profile of these 5-HT receptors is different from those of any known mammalian 5-HT receptor, although they showed some similarities to the 5-HT1A, 5-HT2, and 5-HT3 receptors, as well as to 5-HT receptors on oocytes of some bivalve molluscs.

17-alpha-Hydroxyprogesterone↗