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PubMed1990

Free-choice responding for ethanol versus water in alcohol preferring (P) and unselected Wistar rats is differentially modified by naloxone, bromocriptine, and methysergide.

The role of opioids, dopamine and serotonin in ethanol (EtOH) reward and preference was investigated in non-deprived, Alcohol-Preferring (P), and genetically heterogenous Wistar rats. Operant responding for ethanol was initiated using sweet-solution substitution procedures. The rats were then trained in 30-min daily sessions to respond for ethanol (10% v/v) versus water under a two-lever, free-choice contingency. All testing was conducted in the absence of water and food deprivation or addition of sweeteners to the ethanol drinking solution. Rats of both strains developed stable preferences in responding for ethanol over water and consumed ethanol at quantities sufficient to produce pharmacologically relevant mean blood alcohol concentrations (P-Rats: 98 +/- 19.6 mg%; unselected Wistars: 41.7 +/- 8.5 mg%). In P-rats, systemic naloxone (NAL; 0.125, 0.25 and 0.5 mg/kg) pretreatments resulted in a dose-dependent suppression in responding for both ethanol and water, but did not alter ethanol preference (expressed as percent ethanol of total intake). In contrast, bromocriptine (BRO; 1.0, 2.0 and 4.0 mg/kg) produced a significant, dose-dependent shift in preference from ethanol toward water by inhibiting responding for ethanol while enhancing water consumption. In unselected Wistar rats, NAL and BRO treatments produced changes in ethanol preference patterns similar to those observed in P-rats. However, compared to P-rats, these changes were smaller and not consistently dose dependent. No changes in ethanol preference and water or ethanol intake were observed with methysergide (MET; 2.5, 5.0, 10.0 mg/kg) in either strain of rat. Together, the results suggest a possible involvement of dopaminergic mechanisms in the reinforcing properties of ethanol.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗
PubMed1978

Antiserotonin treatment of hyperprolactinemic amenorrhea: long-term follow-up with metergoline, methysergide, and cyproheptadine.

Twenty patients affected by hyperprolactinemic amenorrhea-galactorrhea have been treated with one or more of the following serotonin antagonists: metergoline, methysergide, and cyproheptadine. Among the 11 patients without evidence of pituitary tumor resumption of menses was observed in five, two of whom had ovulatory cycles; one patient became pregnant; ovulations occurred only during treatment with metergoline. In the group of nine patients with enlarged sellae, three experienced isolated episodes of bleeding, while two had three and four menses each, respectively; all cycles were anovulatory. Plasma prolactin levels and galactorrhea were favorably affected by treatment only in a minority of amenorrhea-galactorrhea patients with and without tumors.

Amenorrhea↗
PubMed1992

Analgesia from the periaqueductal gray in the developing rat: focal injections of morphine or glutamate and effects of intrathecal injection of methysergide or phentolamine.

The aim of these experiments was to examine the changes in antinociception elicited by morphine or glutamate stimulation of the periaqueductal gray of the midbrain (PAG) during the postnatal development of the rat. Pups, aged 3, 10, and 14 days, were implanted with cannulas aimed at either the dorsal or the ventral aspect of the PAG, and glutamate (vehicle, 60 mM or 180 mM) or morphine (vehicle, 2 micrograms or 6 micrograms) was microinjected into one of those two sites. Pups were tested for analgesia against noxious thermal and mechanical stimuli. Morphine produced analgesia at 3 and 10 days of age only when administered to the ventral part of the PAG and the thermal noxious stimulus was tested. Conversely, analgesia induced by glutamate was seen at 3 and 10 days of age only when glutamate was given to the dorsal aspect of the PAG and the mechanical stimulus was used. In 14-day-old pups, both drugs produced analgesia against both types of noxious stimuli regardless of their site of administration within the PAG. Systemically administered naloxone attenuated the analgesic effects of both drugs when they were administered to the ventral PAG, but did not consistently attenuate the analgesic effect of either compound given to the dorsal aspect of the PAG. When either morphine or glutamate was injected into the ventral PAG, intrathecal injections of methysergide attenuated analgesia against the thermal stimulus to a significantly greater degree than the mechanical stimulus and intraspinal injection of phentolamine attenuated analgesia against the mechanical stimulus more potently. When glutamate was given to the dorsal PAG, analgesia against both stimulus types was significantly attenuated. These results indicate that the morphine- and glutamate-induced analgesia mediated by the PAG are developmentally differentiated. These ontogenetic differences most likely reflect differences in the mechanism of action by which these drugs produce analgesia when administered to the PAG, as well as neuroanatomical differences within the dorsal and the ventral regions of the PAG.

Aging↗
PubMed1978

The effects of p-chlorophenylalanine, reserpine, methysergide and cyproheptadine on the dopa-induced EEG synchronization in the rat.

The actions of drugs interfering with central indolaminergic mechanisms were assessed on the Dopa-induced EEG synchronization in the rat. The increased slow wave activity observed during the first 30 min following Dopa (100 mg/kg) was significantly decreased by p-chlorophenylalanine (400 mg/kg), reserpine (4 and 8 mg/kg) and methysergide (16 mg/kg). Cyproheptadine was ineffective in this respect. Our findings lend support to the hypothesis that the initial synchronization after Dopa is related to the release of 5-hydroxytryptamine.

Animals↗
PubMed1981

Influence of naloxone and methysergide on the analgesic effect of clomipramine in rats.

The effects of the tricyclic antidepressant clomipramine were studied in two analgesic tests in rats: (1) vocalization threshold response; and (2) scored behavioral response to electric shock to the tail. Clomipramine (20-50 mg/kg i.p.) produced analgesia, decreasing behavioral response scores and increasing vocalization threshold. Morphine also reduced the response scores in the second test. Naloxone (0.8 mg/kg i.p) or methysergide (20 mg/kg i.p.) (no effect when given alone) abolished the analgesic effect of clomipramine as evaluated by vocalization threshold response. Naloxone alone (0.6 or 2 mg/kg i.p.) increased the behavioral response at 20 and 30 V but did not modify the score at 40 V. Naloxone reduced the analgesic effect of clomipramine or morphine in the behavioral test. These results suggest that the analgesic effect of clomipramine could involve both serotonergic and endorphin central systems.

Analgesics↗
PubMed1990

Microiontophoresis of cocaine, desipramine, sulpiride, methysergide, and naloxone in habenula and parafasciculus.

The effects of microiontophoretically applied cocaine, desipramine (DES), sulpiride (SUL), methysergide (METH), and naloxone (NAL) on the responses of physiologically identified single neurons in the habenula (Hab) and parafasciculus thalami nucleus (PF) were examined in rats. Three cell types were identified in both nuclei on the basis of the responses obtained following noxious stimulation that were classified as "nociceptive-on," "nociceptive-off," and "nonnociceptive" cells. Administration of cocaine generally resulted in a decrease in the firing rate of nociceptive-on and nonnociceptive neurons in both Hab and PF. In contrast, cocaine generally induced an excitation in the baseline firing of the nociceptive-off cells. Cocaine application concomitant with noxious stimulation prevented the evoked responses of the nociceptive-on and the nociceptive-off cells. DES, when applied alone, was found to induce excitation in neuronal discharge of all three cell types in both sites. Combined application of cocaine with DES resulted in no observable change in discharge frequency for the nociceptive-on and nonnociceptive cells, while inducing an additive excitatory effect on the nociceptive-off cells. SUL, in contrast, induced no observable effect on baseline firing when given alone, yet consistently antagonized cocaine-induced effects on all three cell types. Finally, METH and NAL induced no effects on baseline firing or cocaine-induced modifications in neuronal discharge frequency.

Animals↗
PubMed1986

Methysergide-induced precipitated withdrawal syndrome in phencyclidine-dependent rats.

Chronic phencyclidine (PCP) administration has been shown to produce tolerance to a number of its pharmacological actions. We have suggested that PCP interacts with the 5-HT2 receptors since it inhibits [3H]spiperone binding to 5-HT2 receptors in vitro. In the present study, we investigated whether methysergide (a 5-HT2 receptor blocker) induces the precipitated withdrawal syndrome in PCP-tolerant rats. The body weight of the rats in the abrupt and precipitated withdrawal groups was significantly lower 5 days and 1-5 days after withdrawal, respectively, than that in the control group. Furthermore, other typical precipitated abstinence syndrome characteristics such as jumping, wet-dog shake and ptosis were also observed in the precipitated withdrawal group. These results suggest that PCP produces its behavioral effects via an agonistic interaction with 5-HT2 receptor sites and that our method may be very useful for the development of a rat model for studying physical dependence on PCP.

Animals↗
PubMed1990

Interaction of thyrotropin-releasing hormone and methysergide on the monosynaptic reflex in isolated mammalian spinal cord.

The interaction between thyrotropin-releasing hormone (TRH) and methysergide (MeSG) on reflex activity was examined in spinal cords from neonatal rats. MeSG depressed the monosynaptic reflex (MSR) by nearly 90% at 0.03 microM but had no effect on the dorsal root reflex at 0.003-3.0 microM. Neither spiperone, ketanserin, cyproheptadine nor ICS 205-930 (3-tropanyl-indole-3-carboxylate) depressed the MSR nor did they affect the potentiation elicited by TRH. TRH reversed the depression of the MSR by MeSG in a concentration-dependent manner without affecting the dorsal root reflex. MeSG-induced depression of the MSR was also reversed by 3,4-diaminopyridine which simultaneously increased the magnitude and duration of both reflexes. It appears that neither MeSG-induced depression nor TRH-induced potentiation of the MSR involves the spinal serotonergic system or blockade of K+ channels.

5,7-Dihydroxytryptamine↗
PubMed1994

Effects of serotonin receptor blockade by methysergide on loaded breathing in the rabbit.

Previous works demonstrated that the excitatory role of serotonin (5-hydroxytryptamine, 5-HT) on ventilation is mediated by 5-HT1,2 receptors stimulation. We hypothesized that load-induced hypoventilation could be minimized by a central release of 5-HT. Conversely, blockade of 5-HT receptors should accentuate hypoventilation. We compared the ventilatory effects of methysergide (MS), a 5-HT1,2 receptors antagonist, in 3 groups of anesthetized, spontaneously breathing rabbits: (1) a group of animals breathing for 60 min through a 370 cm H2O.liter-1.s inspiratory resistive load (IRL group), whose paCO2 increased with IRL; (2) a Control group; (3) a Control + CO2 group, made hypercapnic to assess the possible effect of this stimulus on the ventilatory responses to MS. In the 3 groups, i.v. injection of MS induced the same ventilatory changes, characterized by a rapid shallow breathing with a shorter integrated diaphragmatic activity. This confirms the tonic facilitatory effect of 5-HT on ventilation and suggests that IRL would not increase 5-HT release in the sites close to the respiratory nuclei.

Animals↗
PubMed1984

LSD but not methysergide reduces the inhibitory effect of the medullary raphe stimulation on the spinal reflex in rats.

Conditioning stimulation of the nucleus raphe in the rat medulla enhanced the monosynaptic reflex (MSR) and depressed the polysynaptic reflex (PSR) in separate time courses. The PSR decreasing effect was reduced in preparations pretreated with reserpine, PCPA, or 5,6-DHT. The MSR increasing effect was not altered by these three pretreatments. Intravenously administered LSD but not methysergide reduced the PSR decreasing effect with no influence on the MSR increasing effect. These two drugs had similar effects on the unconditioned responses; the MSR was decreased and the PSR was increased. Thus, the PSR decreasing effect seems to be mediated via a serotonergic pathway probably descending from the nucleus raphe.

Animals↗
PubMed1991

The effects of intracerebroventricular injection of naloxone, phentolamine and methysergide on the transmission of nociceptive signals in rat dorsal horn neurons with convergent cutaneous-deep input.

In anaesthetized rats, recordings were made from nociceptive dorsal horn neurons with convergent input from the skin and deep somatic tissues. The results of a previous study have shown that in these neurons the input from deep nociceptors is subjected to a much stronger tonic descending inhibition than is the input from cutaneous nociceptors. The aim of the present study was to find out whether at supraspinal levels opioidergic, adrenergic, or serotoninergic transmitters are involved in this quite specific inhibition of deep nociception. Injections of naloxone, phentolamine, and methysergide into the third ventricle showed that only naloxone is capable of abolishing the tonic inhibition of the deep nociceptive input to spinal neurons. The input from cutaneous nociceptors to the same cells was largely unaffected by naloxone. Thus the effects of intracerebroventricular injection of naloxone resembled those obtained with a spinal cold block in a previous study; with the exception that the increase in background activity--which is prominent during cold block--was missing after the injection of naloxone. The present results demonstrate that the tonic descending inhibition of the deep nociception operates with opioidergic synapses at the supraspinal level. In contrast, supraspinal adrenergic and serotoninergic mechanisms do not appear to contribute to the tonic inhibition. The data confirm and extend previous results which suggested that a particular portion of the descending antinociceptive system may act mainly on the input from deep nociceptors. Pharmacologically, this particular portion seems to be opioidergic in nature.

Animals↗
PubMed1976

Facilitation of receptivity in estrogen-primed rats during successive mating tests with progestins and methysergide.

The role of hormonal and experiential variables in mediating the gradual increase of receptivity occurring during weekly tests was evaluated in adult ovariectomized females. Hormone treatment consisted of estradiol benzoate (EB) injection followed by progesterone (P), 20alpha-hydroxyprogesterone (20alpha-OHP), methysergide maleate (Me), or oil during weekly mating tests. The experiential conditions were vaginal stimulation, mounts only, or no interaction with males. There was a gradual increase in receptivity in all groups even en the one receiving oil. Progressive facilitation occurred even when no interaction with the male was permitted. Interchanging the synergists on the sixth and seventh tests was not detrimental to the display of receptivity attained with synergists given previously. Thus, we concluded that successive injections of EB rather than synergists or experience mediate this increase in receptivity.

Animals↗
PubMed1986

Methylergometrine, an active metabolite of methysergide.

In conscious dogs methysergide (MS) caused constriction of the saphenous vein at about 3000 times lower doses than methylergometrine (MT) when infused locally, but it elicited only a short-lasting venoconstrictor response when injected systemically intravenously. MS and MT proved to be equally active venoconstrictor agents when administered orally. Analysis of canine plasma by high-performance liquid chromatography showed that after both oral and intravenous administration of MS large amounts of MT appeared in the plasma, whereas only low and transient levels of MS could be detected. It is suggested that one of the first steps in metabolism of MS is demethylation at position 1 of the indole, leading to the formation of MT, which may be a main active principle of the therapeutic effectiveness of MS in the interval treatment of migraine headache.

Administration, Oral↗
PubMed1998

Cough headache responsive to methysergide.

Cough headache is a very distinct syndrome of headache precipitated by coughing, lifting, bending, sneezing, laughing, or straining. The pain can be severe and, if precipitation is difficult to avoid, certainly distressing. The usual treatment is indomethacin, which can be highly effective although recently lumbar puncture has again been advocated. We encountered a patient in whom indomethacin use was relatively contraindicated and who had an apparent response to methysergide.

Aged↗
PubMed1994

Ethanol consumption following acute treatment with methysergide, fluoxetine, fenfluramine, and their combination.

Methysergide (MS), a postsynaptic serotonin antagonist, was administered acutely in three experiments in relation to water or 5% ethanol solution intake of 24-hr, water-deprived male Sprague-Dawley rats. In the first experiment, MS significantly increased the consumption of ethanol at doses of 0.25, 2.0, and 4.0 mg/kg. Water intake was significantly increased by MS at the 2.0 mg/kg dose. In the second experiment, which was different from the first one in that MS was administered during the dark cycle, ethanol solution intake was again significantly increased at all three levels. In the third experiment, fenfluramine (FFL) and fluoxetine (FLU) were administered acutely (at 8 mg/kg) after MS (0.25 mg/kg) followed by measuring water or ethanol solution intake. FFL and FLU significantly decreased intake of both water and ethanol solution, a process that was significantly reversed by MS; to a greater degree for FLU (74%) than for FFL (57%). The successful use of MS in increasing ethanol intake in these studies may be due to the low doses used in comparison with earlier unsuccessful attempts. The procedure of treating 24-hr, water-deprived rats with acute doses of pre- and postsynaptic serotonin agonists and antagonists appears to be a useful model for further elucidation of their interaction in ethanol consummatory behavior.

Alcohol Drinking↗
PubMed1991

5-hydroxytryptamine antagonistic effects of ICI 169,369, ICI 170,809 and methysergide in human temporal and cerebral arteries.

ICI 169,369 and ICI 170,809 are two chemically novel 5-HT antagonists that have high affinity for the 5-HT2 binding site in rat cortex (Ki 1.79 x 10(-8)M and 6.6 x 10(-10)M, respectively). In human temporal artery preparations ICI 169,369 was shown to cause a progressive rightward shift of the 5-HT-response curve over the range 10(-7)-10(-5)M, while ICI 170,809 in these concentrations shifted the curve to the same degree (no dose dependency). In human cerebral vessels no effect was observed until a high concentration (10(-5)M) was used for either compounds. The mixed 5-HT1/5-HT2 antagonist, methysergide, induced a non parallel rightward shift of the 5-HT-induced concentration-effect curve with a depression of the maximum achievable response in both the temporal and cerebral artery. The mode of effect of ICI 169,369 and ICI 170,809 to block the 5-HT-induced contractions in human temporal vessels resembles that of the pure 5-HT2 antagonist ketanserin, thus suggesting that the two ICI compounds are mainly 5-HT2 antagonists. In high concentrations both ICI 169,369 and ICI 170,809 have vasorelaxant properties, explaining the reduction in maximum 5-HT-induced contraction seen at high antagonist concentrations.

Cerebral Arteries↗
PubMed1970

Pleural effusion and fibrosis during treatment with methysergide.

Two patients being treated for migraine with methysergide developed extensive pleural fibrosis, and in addition one of them had bilateral pleural effusions, After treatment was stopped these complications, which are thought to have been due to the drug, cleared in the next few months.

Adult↗