SEARCH · PubMed Health

Results for “Metergoline”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources

PubMed1989

Obsessive-compulsive disorder as a 5-HT subsystem-related behavioural disorder.

Involvement of the brain serotonin (5-HT) neurotransmitter system in obsessive-compulsive disorder (OCD) was originally suggested on the basis of therapeutic effects found with the semiselective serotonin uptake inhibitor, clomipramine. More recent studies directly comparing clomipramine with non-selective or norepinephrine-selective uptake inhibitors, such as desipramine or nortriptyline, as well as studies with new, more selective serotonin uptake inhibitors, including fluvoxamine and fluoxetine, have supported that hypothesis. Clomipramine's antiobsessional effect has been augmented with the serotonin precursor, L-tryptophan, or with lithium, which has prominent serotonergic effects. Patients whose OCD symptoms improved on clomipramine worsened when the drug was discontinued (regardless of duration of therapy) and improved when clomipramine was reinstituted. OCD symptoms also worsened when metergoline, a 5-HT antagonist, was given to patients who had improved with clomipramine. Metergoline given alone had no effect. Administration of m-chlorophenylpiperazine (m-CPP), a 5-HT receptor agonist, to untreated OCD patients increased their anxiety, depression, and dysphoria, and exacerbated their OC symptoms. After 4 months of clomipramine therapy, m-CPP failed to produce the same behavioural effects, suggesting an alteration of a 5-HT subsystem (possibly downregulation of some 5-HT receptors). The data reviewed suggest an important role for an abnormal brain 5-HT subsystem in patients with OCD.

Brain↗

PubMed1989

Reduction of food intake by manipulation of central serotonin. Current experimental results.

Serotonergic anorectics are correctly defined only if they enhance 5-HT transmission and have their anorectic effects inhibited by drugs that block 5-HT receptors. Fenfluramine, the prototype indirect 5-HT agonist, and its metabolite, norfenfluramine, act as 5-HT releasers and uptake inhibitors and are both more effective in the dextro form. They lack the stimulant activity and do not cause hyperthermia or stereotypical behaviour as is characteristic of amphetamines. The anorectic effect of those drugs is attenuated by metergoline, a 5-HT receptor antagonist, in animals and man; 5-HT uptake inhibitors such as fluoxetine, zimelidine, SL 810385, and sertraline also cause anorexia, but only sertraline antagonism by metergoline has been reported. The effect of serotonergic anorectics on 5-HT release has been poorly investigated. Quipazine and RU-24969 cause anorexia by acting directly on 5-HT post-synaptic receptors. Serotonergic nerve terminals take up [3H]-D-fenfluramine and bind with high affinity in rat brain; uptake, an active process, appears to occur at a different site than binding, which is not affected by ouabain or low temperature. Anorexia is probably induced by interaction with 5-HT1B receptors in the rat; the human equivalent of this receptor is not known, but the 5-HT1D type is a likely candidate.

Animals↗

PubMedDate not supplied

Effect of chloro-N-desmethyldiazepam on serum and brain tryptophan and serotonin in relation to the activity of central serotonergic neurons.

Chloro-N-desmethyldiazepam (CDD) significantly reduced plasma tryptophan (TRY) and increased brain TRY in mice and rats. Quipazine did not change TRY levels in mouse plasma and brain but it respectively reduced and increased these two parameters in rats, to almost the same extent as CDD. Metergoline, an antagonist of serotonergic receptors, decreased blood TRY in both mice and rats but failed to change brain TRY. CDD significantly but slightly increased brain serotonin in rats. This effect was blocked by metergoline.

Animals↗

PubMed1998

Discriminative stimulus characteristics of BMY 14802 in the pigeon.

Pigeons were trained to discriminate intramuscular injections of 5.6 mg/kg BMY 14802, a drug that has relatively high affinity for sigma binding sites, from saline in a two-key operant procedure. Many compounds that displace sigma binding failed to produce BMY 14802-like discriminative stimulus effects; these included (+)-SKF 10,047, (+)3-PPP, DTG and MR 2035; the typical antipsychotic haloperidol; the putative antipsychotics tiospirone, cinuperone and rimcazole; and the uncompetitive NMDA antagonist phencyclidine. In addition, MR 2035 and tiosperone failed to antagonize the discriminative stimulus effects of BMY 14802. The selective D2 antagonist eticlopride and the norepinephrine uptake blocker and antidepressant desmethylimipramine also failed to evoke substantial BMY 14802-appropriate responding. In contrast to sigma ligands and other reference compounds, the 5-HT1A agonists buspirone, 8-OH-DPAT and spiroxatrine dose-dependently produced BMY 14802-like discriminative stimulus effects. The limited-efficacy 5-hydroxytryptamine (HT)1A agonist NAN 190 did not produce BMY 14802-like discriminative effects; however, it did competitively antagonize the stimulus effects of BMY 14802 and the BMY 14802-like stimulus effects of (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin. Other serotonergic compounds failed to produce substantial BMY 14802-appropriate responding; such as 5-HT1 agonist I-5-HTP; 5-HT1A/1B agonist RU24969; 5-HT1B/1C agonist m-CPP; 5-HT1C/2 agonist quipazine; 5-HT1C/2 antagonists, metergoline and the atypical antipsychotic clozapine; and 5-HT3 antagonist ondansetron. Also, metergoline, ondansetron and pirenpirone failed to antagonize the stimulus effects of BMY 14802. These results indicate that the discriminative stimulus effects of BMY 14802 are serotonergically mediated primarily by 5-HT1A receptors rather than by sigma sites.

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

PubMed1987

Rats and marmosets respond differently to serotonin agonists and antagonists.

The actions of the serotonin precursor 5-hydroxytryptophan (5-HTP), the agonist 5-methoxy-N,N-dimetyltryptamine (MeODMT) and quipazine (QPZ) and the antagonists cyproheptadine, methysergide and metergoline, were studied in the rat and in the common marmoset (Callithrix jacchus). The precursor and agonists elicited head shakes, forepaw padding, splayed hindlimbs, tremor and Straub tail in the rat. However, head shakes were not observed after MeODMT and Straub tail was not observed after QPZ. Carbidopa plus 5-HTP potentiated only head shakes, while tranylcypromine (TCP) plus 5-HTP potentiated all the behaviors above. In the marmoset, the action of these drugs elicited drowsiness, teeth chattering, ataxia, vomiting and decreased motor activity, although vomiting was not elicited by MeODMT and ataxia and drowsiness by QPZ. Although TCP plus 5-HTP potentiated all these behaviors, carbidopa plus 5-HTP was not effective. Rats treated with the antagonists (1.0, 5.0 and 10 mg/kg doses) did not show any of these behaviors, but marmosets treated with the same drugs developed "drowsiness", vomiting, and decreased motor activity; nonetheless, cyproheptadine (5.0 and 10 mg/kg doses) did not elicit "drowsiness", while increasing motor activity and the number of head shakes. Pretreatment of marmosets with these antagonists blocked only teeth chattering elicited by MeODMT (4.0 mg/kg) and QPZ (10 mg/kg). Pretreatment with haloperidol, p-chlorophenylalanine and alpha-methyl-P-tyrosine had no effect. The data obtained show that rats and marmosets present differential behavioral responses to the 5-HT drugs used.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Receptor blocking drugs and amphetamine anorexia in human subjects.

The interaction between the receptor antagonist thymoxamine (THYM), propranolol (PPL) and metergoline (MTG) with dexamphetamine (d-Amp)-induced anorexia was examined in a series of studies in normal female volunteers. Visual analogue scale (VAS) ratings of hunger were made and food intake was measured using an automated solid food dispenser (AFD). d-Amp (10 mg) significantly depressed hunger ratings compared to placebo in two of the three studies and its effect was countered by the addition of MTG (4 mg). d-Amp significantly reduced food intake compared to placebo in two studies. In all trials the reduction in food intake following d-Amp was significantly greater than would have been predicted from its effect on hunger. THYM (160 mg) and PPL (40 mg) were associated with no changes in food intake when given alone or with d-Amp, MTG increased food intake (but not significantly) and the combined effects of MTG and d-Amp was the algebraic sum of the effect of each; but there appeared to be no true pharmacological interaction between blocker and anorectic. The results indicated that there may be some dissociation between the effect of d-Amp on hunger and food intake but have failed to produce evidence that noradrenergic pathways are involved. The results are consistent with the theories that d-Amp anorexia does not involve the release of 5-hydroxytryptamine (5-HT) but that 5-HT pathways are involved in the feeding process.

Adult↗

PubMed1991

Species differences in presynaptic serotonin autoreceptors: mainly 5-HT1B but possibly in addition 5-HT1D in the rat, 5-HT1D in the rabbit and guinea-pig brain cortex.

The pharmacological properties of presynaptic serotonin autoreceptors were compared in slices of rat, rabbit, and guinea-pig brain cortex. The slices were preincubated with 3H-serotonin and then superfused with medium containing fluvoxamine 3 mumol/l and stimulated four times by trains of four pulses delivered at 100 Hz. Cumulative concentration-response curves were determined and used for the calculation of agonist EC50 values and maximal effects and antagonist KB values. Unlabelled serotonin itself and the serotonin receptor agonists 5-carboxamidotryptamine (5-CT), 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridinyl)-1H-indole (RU 24969) and (+/-)-8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) reduced the stimulation-evoked overflow of tritium with a rank order of potency 5-CT = RU 24969 greater than serotonin greater than 8-OH-DPAT in the rat and 5-CT greater than serotonin greater than RU 24969 greater than 8-OH-DPAT in the rabbit and guinea-pig. Ipsapirone caused no change. Metitepine and metergoline antagonized the effect of 5-CT; the KB values were lower in the rabbit and guinea-pig than in the rat. Yohimbine at up to 1 mumol/l did not reduce the evoked overflow of tritium and did not antagonize the inhibitory effect of 5-CT in the rat but reduced the evoked overflow in the rabbit and counteracted the effect of 5-CT in the guinea-pig. (-)-Propranolol, conversely, reduced the evoked overflow of tritium in the rat but neither reduced the evoked overflow nor antagonized the effect of 5-CT in the rabbit and guinea-pig. Isamoltane did not significantly change the effect of 5-CT in any species. In the rat, it also failed to antagonize the inhibitory effect of 8-OH-DPAT but did antagonize the effect of RU 24969. The inhibition caused by 8-OH-DPAT persisted in the presence of idazoxan but was attenuated by metitepine in all species. The experimental conditions used permit the determination of the constants of agonist and antagonist action undistorted by autoinhibition. The results confirm the view that the serotonin axons of rat brain possess 5-HT1B autoreceptors. They show by direct comparison under identical conditions that the autoreceptors in rabbit and guinea-pig are very similar to each other but differ markedly from those in the rat. The results give additional credence to previous suggestions that, in the rabbit and guinea-pig, the autoreceptors are 5-HT1D. The serotonin axons of rat brain cortex may possess 5-HT1D in addition to 5-HT1B autoreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Dorsal raphé stimulation modifies striatal-evoked antidromic invasion of nigral dopaminergic neurons in vivo.

Extracellular single unit recordings were obtained from antidromically identified nigrostriatal dopaminergic neurons in anesthetized rats to determine the effects of dorsal raphé stimulation on the somatodendritic excitability of substantia nigra dopaminergic neurons. Stimulation of the dorsal raphé with a brief train of pulses delivered 7-2 ms prior to the neostriatal-evoked antidromic response significantly reduced the proportion of neostriatal-evoked antidromic responses that consisted of both initial segment and somatodendritic components without significantly altering the neostriatal-evoked post-stimulus inhibitory period. Raphé stimulation alone facilitated post-stimulus neuronal firing in almost half of the cells examined. The raphé-induced decrease in somatodendritic excitability was blocked by the serotonin antagonist, metergoline (0.5-2.0 mg/kg, i.v.), without significantly affecting the rate or pattern of spontaneous activity. The tryptophan hydroxylase inhibitor, parachlorophenylalanine (400 mg/kg, i.p. for three consecutive days), abolished the decrease in somatodendritic excitability following raphé stimulation which could be re-instated by intravenous administration of 5-HTP. The dopamine antagonists haloperidol (25-100 micrograms/kg, i.v.) and sulpiride (10-30 mg/kg, i.v.) also blocked the effects of dorsal raphé stimulation on somatodendritic invasion. These data suggest that in vivo, serotonin liberated from raphé-nigral terminals facilitates the release of dopamine from nigrostriatal dendrites resulting in a local, autoreceptor-mediated reduction in somatodendritic excitability without affecting the spontaneous firing rate and excitability of the neuron as a whole.

Animals↗

PubMed1980

Further evidence for an inhibitory role of central 5-HT in male rat sexual behavior.

The 5-hydroxytryptamine (5-HT) reuptake inhibitors zimelidine (10 mg/kg IP 1.5h pretest) or alaproclate (20 mg/kg IP 1.5h pretest) produced a prolongation of the ejaculation latency and of the post-ejaculatory interval in male rats treated with a subthreshold dose of 5-hydroxytryptophan (5-htp) (12.5 mg/kg IP 1h pretest). The 5-HTP-induced (50 mg/kg IP 1h pretest) prolongation of ejaculatory latency was effectively counteracted by administration of the 5-HT receptor blocking agent metergoline (1 mg/kg IP 1.5h pretest). All animals were treated with an inhibitor of peripheral aromatic amino acid decarboxylase, indicating that the effects are of central origin. The results support the contention that central 5-HT plays an inhibitory role in male rat sexual behavior.

5-Hydroxytryptophan↗

PubMed1985

Anti-aversive role of serotonin in the dorsal periaqueductal grey matter.

Microinjection of 5, 10, and 20 nmol serotonin (5-HT) and of 0.5, 1, and 2 nmol 5-methoxy-N, N-dimethyltryptamine (5-MeODMT) into the dorsal midbrain of rats bearing chronically implanted chemitrodes raised the electrical threshold for inducing escape behaviour following stimulation of the dorsal periaqueductal grey matter (DPAG). Linear regressions of log dose against drug-induced increase in aversive threshold were obtained for 5-HT and 5-MeODMT. The 5-MeODMT dose-effect curve was steeper and lay to the left of the 5-HT dose-effect curve. Local pre-treatment with 10 nmol metergoline or ketanserin blocked the anti-aversive effect of 10 nmol 5-HT, whereas pre-treatment with 100 nmol zimelidine potentiated this effect of 5-HT. The same dose of zimelidine raised the aversive threshold when given alone. These results suggest that 5-HT plays an inhibitory role in the DPAG controlling aversion, probably mediated by 5-HT2 receptors.

Animals↗

PubMed1985

Effects of 8-OH-DPAT, lisuride and some ergot-related compounds on the acoustic startle response in the rat.

Five ergot-related compounds were examined for their effects on the acoustic startle response in the rat. The startle amplitude and the startle latency were registered. 8-Hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT; 0.5-8 mg/kg) and lisuride (0.05-0.8 mg/kg) were found to enhance the startle amplitude, while the mainly DA receptor active ergot derivatives pergolide (0.2-0.8 mg/kg), bromocriptine (5-20 mg/kg) and LY 141865 (5-20 mg/kg) had no, or even the reverse, effect. All five compounds caused a prolongation of the startle latency. The increased startle amplitude caused by 8-OH-DPAT (2 mg/kg) and lisuride (0.2 mg/kg) was successfully antagonized by the 5-HT receptor antagonist methiothepin (0.1 mg/kg) but not by metergoline (1 mg/kg). 5-Hydroxy-L-tryptophan (L-5-HTP; 12.5-50 mg/kg), administered to pargyline- and benserazide-pretreated animals, was included for comparison. The serotonin precursor caused a marked increase in the startle amplitude and a shortening of the startle latency.

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

PubMed1981

Involvement of the amygdala in the effect of antidepressants on the passive avoidance deficit in bulbectomised rats.

In the present study the role of the amygdala is demonstrated in the effect of antidepressant drugs on passive avoidance learning in bulbectomised rats. Imipramine, amitriptyline, or fluoxetine injected bilaterally (2 X 10 microgram) into the medial part of the amygdala improves passive avoidance learning by bulbectomised rats. Systemic pretreatment with metergoline attenuates the effect of local imipramine or fluoxetine injection. Microinjection of serotonin but not noradrenaline into the amygdala improves passive avoidance learning by bulbectomised rats. The relevance of the amygdala in the behavioral effects of antidepressants in animals is discussed.

Amitriptyline↗

PubMed1981

Chronic treatment with some atypical antidepressants increases the brain level of 3-methoxy-4-hydroxyphenylglycol (MHPG) in rats.

We examined the effects of some atypical antidepressants with central antiserotonergic activity (mianserin, trazodone, danitracen, pizotifen), and 5-HT receptor blocking agents (cyproheptadine and metergoline), on whole rat brain levels of the main noradrenaline (NA) metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG). In acute experiments, when drugs were injected in a single dose 1, 2, 4, 24 or 48 h before decapitation, only mianserin elevated the MHPG level. In chronic experiments (drugs given b. i. d. for 3 weeks, the last dose being given 4 or 48 h before decapitation), all the drugs significantly increased the concentration of whole brain MHPG. The results indicate that chronic administration of atypical antidepressants leads to activation of the central NA system. It seems, with the exception of mianserin, that this is a secondary phenomenon, resulting from the antiserotonergic activity of the drugs. Our results further corroborate the existence of a serotonergic-noradrenergic interaction, consisting of an inhibitory influence of serotonin on the noradrenergic system.

Animals↗

PubMed1989

Evidence that d-fenfluramine anorexia is mediated by 5-HT1 receptors.

The effects of eight serotonin (5-HT) receptor antagonists on the anorectic effect of d-fenfluramine (3.0 mg/kg, IP) were examined in a test of sweet mash consumption, using non-deprived male rats. d-Fenfluramine's effect was attenuated by the mixed 5-HT1/5-HT2 receptor antagonists, methiothepin and metergoline; by the 5-HT2 receptor antagonist ritanserin; and by (+/-)cyanopindolol, a mixed 5-HT1A/5-HT1B receptor antagonist. In contrast, d-fenfluramine's effect was not antagonised by the 5-HT2 receptor antagonists ketanserin and ICI 169 369; the 5-HT3 receptor antagonist ICS 205 930; or by xylamidine, a peripheral 5-HT receptor antagonist. In this feeding model, none of the 5-HT antagonists, when tested alone, had any effect to increase palatable food consumption. The pattern of results obtained strongly suggest that central 5-HT1 receptors play an important role in the mediation of d-fenfluramine-induced anorexia.

Amidines↗

PubMed1989

Behavioral effects of (+-) 3,4-methylenedioxyamphetamine (MDA) and (+-) 3,4-methylenedioxymethamphetamine (MDMA) in the pigeon: interactions with noradrenergic and serotonergic systems.

The effects of three amphetamine analogs were assessed in pigeons key pecking under a multiple 3-min fixed-interval (FI), 30 response fixed-ratio (FR) schedule of food presentation. At doses between 0.1 and 10.0 mg/kg, (+-) 3,4-methylenedioxyamphetamine (MDA), (+-) 3,4-methylenedioxymethamphetamine (MDMA), and (+-)-N-ethyl-3,4-methylenedioxyamphetamine (MDE) either had no effect or decreased response rates in both components of the multiple schedule in a dose-dependent manner. MDA was at least 1 log unit more potent than the other two compounds. Metergoline (0.1-1.0 mg/kg), a serotonin (5-HT) antagonist with comparable affinity for the 5-HT1 and 5-HT2 receptor subtypes, blocked the rate-decreasing effects of 3.0 mg/kg MDA in both components of the multiple schedule, but did not affect the MDMA dose-response curve. The 5-HT2 receptor antagonist ketanserin (0.1-3.0 mg/kg) also restored FI and FR responding that was decreased by 3.0 mg/kg MDA, but had no effect on responding suppressed by MDMA. The noradrenergic alpha-1 antagonist prazosin (0.3-3.0 mg/kg) blocked the behavioral effects of 3.0 mg/kg MDMA at doses that did not attenuate MDA's rate-decreasing effects. These results indicate that although MDA and MDMA are structurally similar and have similar behavioral effects, their actions appear to be mediated through different neurotransmitter systems.

3,4-Methylenedioxyamphetamine↗

PubMed1984

In vivo increase in hypothalamic cyclic AMP following 5-hydroxytryptophan administration in rats.

The administration of 5-hydroxytryptophan (5-HTP, 100 mg/kg, i.p.) consistently increased hypothalamic cyclic AMP levels in rats treated 10 days earlier with the serotonin neurotoxin, 5,7-dihydroxytryptamine (5,7-DHT), to produce 5-HT receptor supersensitivity. However 5-HTP (100 mg/kg), failed to cause an increase in hypothalamic cyclic AMP in rats not pretreated with 5,7-DHT. The 5-HTP-induced increase in cyclic AMP was blocked by the decarboxylase inhibitor, benserazide (RO 4-4602, 800 mg/kg) and by the 5-HT antagonist metergoline (5 mg/kg). Other treatments that caused a significant elevation of hypothalamic cyclic AMP included: (a) L-Tryptophan plus the monoamine oxidase inhibitor, tranylcypromine, and (b) the serotonin agonist, 1-(m-trifluromethylphenyl)-1-piperazine. The 5-HT antagonist, methysergide, blocked the serotonin receptor mediated behavioral syndrome, but failed to prevent the increase in hypothalamic cyclic AMP. Moreover, the 5-HT agonist, 5-methoxy-N, N-dimethyltryptamine, (5-Me-DMT), induced a strong behavioral syndrome but failed to significantly increase hypothalamic cyclic AMP. These findings suggest that activation of 5-HT receptors somewhere in the brain causes an increase in hypothalamic cyclic AMP, but further studies will be needed to determine whether this is a direct result of activation of the 5-HT receptors in the hypothalamus.

5,7-Dihydroxytryptamine↗

PubMed1983

Studies on the role of serotonin in different regions of the rat central nervous system on pentylenetetrazol-induced seizures and the effect of di-n-propylacetate.

5,7-Dihydroxytryptamine (5,7-DHT) injections which caused selective depletion of serotonin in the forebrain enhanced the seizures caused by pentylenetetrazol (PTZ 90 mg/kg s.c.) in rats. No effect was observed in rats with 5,7-DHT-induced depletion of spinal serotonin or treated with metergoline (1 mg/kg i.p.) or methysergide (10 mg/kg i.p.). The various procedures aimed at decreasing serotonin transmission did not significantly modify the effect of di-n-propylacetate (DPA) on tonic seizures and mortality caused by PTZ but significantly reduced the DPA-induced increase in the latency to the first convulsion. More animals with clonic seizures were seen in the DPA-treated group which had been subjected to selective depletion of spinal serotonin or treated with methysergide than in DPA-treated controls. Combined treatment with d-fenfluramine (1.25 mg/kg i.p.) and DPA (75 mg/kg i.p.), doses which by themselves had no significant effect, reduced tonic seizures and mortality caused by PTZ. The results show that a diffuse deficit in forebrain serotonin enhances PTZ-induced seizures. Serotonin does not play an important role in the effect of DPA against PTZ-DPA on clonic convulsions. Agents increasing serotonin transmission may enhance the anticonvulsant activity of DPA.

5,7-Dihydroxytryptamine↗

PubMed1990

Effects of 5-hydroxytryptamine on the firing rates of neurons of the lateral vestibular nucleus in the rat.

5-hydroxytryptamine (5-HT) was delivered microiontophoretically (20-80 nA) to cells of the lateral vestibular nucleus of anaesthetized rats to test its influence on the spontaneous activity of single neurons. 5-HT increased the rate of firing of 94% of the units tested. The enhancement persisted for up to 700 s after the end of the 5-HT ejection and the maximum magnitude of the excitation (10-3400%) showed a hyperbolic correlation (rho = 0.86) with background firing. In 43% of units the enhancement was preceded by a short-lasting (less than 105 s) depression of the neuronal firing rate, the magnitude of which was unrelated to the background mean firing rate. Both components of the 5-HT response were dose-dependent. Only the excitatory responses were antagonized by metergoline, methysergide and ketanserin. The putative 5-HT agonist, 5-methoxy-N,N-dimethyltryptamine, applied microiontophoretically, depressed the background firing rate and was not antagonized by methysergide. These results demonstrate that 5-HT modifies the responsiveness of vestibular neurons and suggest that at least two mechanisms and maybe two types of receptors are activated by 5-HT in this nucleus.

Action Potentials↗