Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Following the IV administration of d-methamphetamine (MA), rats showed slow head shaking (SHS) and stereotyped gnawing (SG) behaviors in a dose-dependent manner. Methysergide, cyrpoheptadine, and p-chlorophenylalanine given intracerebroventricularly (ICV) or systemically significantly blocked SHS behavior induced by 10 mg/kg MA. Combined administration of L-5-hydroxytryptophan and peripheral decarboxylase inhibitor (Ro 4-4602) enhanced SHS behavior. Tyrosine hydroxylase inhibitor (H44/68) blocked SG behaviors, but dopamine-beta-hydroxylase inhibitors (FLA 63 and U-14, 624) and combined administration of L-3,4-dihydroxyphenylalanine and Ro-4-4602 enhanced it. These drugs did not affect SHS behavior. Phentolamine, phenoxybenzamine, clonidine, isoproterenol, and propranolol given ICV or systemically showed no effect on either SHS or SG behaviors. These results suggest that SHS behavior is produced by the activation of seronergic neurons in the central nervous system and are consistent with the view that SG behaviors are mediated through the release of dopamine. Some neuroleptics inhibited SHS as well as SG behaviors, but the older of inhibitory activity of neuroleptics onSHS behavior was quite different from their effects on SG behaviors induced by MA or apomorphine.
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PMID:The involvement of serotonergic neurons in the central nervous system as the possible mechanism for slow head-shaking behavior induced by methamphetamine in rats. 11 84

Pharmacological stimulation of central serotonin (5-HT) receptors causes a behavioral syndrome characterized by simultaneous side-to-side head weaving or head tremor, forepaw padding and splayed hindlimbs. This syndrome has been proposed and used as a model for 5-HT receptor activity. Questions have been raised about the possible involvement of catecholamines. This study was designed to differentiate behavioral signs contributed by 5-HT from those that might be due to catecholamines. Depletion of catecholamines by alpha-methyl-p-tyrosine, or depletion of 5-HT by either p-chlorophenylalanine or 5,7-dihydroxytryptamine, did not prevent the syndrome caused by 5-methoxy-N,N-dimethyltryptamine, a 5-HT receptor agonist. Pretreatment with methysergide, but not phenoxybenzamine or pimozide, prevented the syndrome caused by 5-methoxy-N,N-dimethyltryptamine. Conversely, 5-HT depletion prevented the syndrome caused by monoamine oxidase inhibitor and levodopa; behavioral response was restored in p-chlorophenylalanine-pretreated rats by 5-hydroxytryptophan. Methysergide prevented the syndrome caused by monoamine oxidase inhibitor and levodopa, but phenoxybenzamine or pimozide did not. Intraventricular 5-HT or dopamine also caused the behavioral syndrome after monoamine oxidase inhibition. p-Chlorophenylalanine pretreatment prevented the syndrome caused by dopamine, but did not prevent the syndrome caused by 5-HT. Our results suggest that systemic levodopa or intraventricular dopamine produces the behavioral signs through 5-HT mechanisms; endogenous catecholamine mechanisms are not involved directly in either the cause or expression of the behavioral syndrome.
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PMID:Specificity of a rat behavioral model for serotonin receptor activation. 68 17

1 A simple method of injecting soluble substances into the lateral ventricle of the brain of the conscious mouse is described. 2 The effect of various doses of noradrenaline, dopamine, acetylcholine, 5-hydroxytryptamine given into the right lateral brain ventricle were tested on locomotor and exploratory activities of mice. 3 Noradrenaline in a dose of 0.1 mug increased locomotor activity. This effect was prevented by phenoxybensamine but not by propranolol. 4 Higher doses of noradrenaline (1 or 10 mug) decreased locomotor and exploratory activities. Propranolol but not phenoxybenzamine abolished these effects. 5 Dopamine (0.1 or 1 mug) increased locomotor activity. The higher doses also induced tremor. 6 The highese dose of dopamine tested (10 mug) elicited stereotypical behaviour. 7 All the behavioural phenomena induced by 0.1 mug and 10 mug of dopamine were blocked by pimozide. 8 Acetylcholine (1 and 10 mug) and 5-hydroxytryptamine (1 mug) inhibited locomotor and exploratory activity. 9 The effects of 1 and 10 mug of acetylcholine were abolished by atropine (5 mg/kg i.p. Methysergide (5 mg/kg i.p.) had no influence on the effects of 5-hydroxytryptamine (1 mug).
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PMID:Behavioural changes induced in conscious mice by intracerebroventricular injection of catecholamines, acetylcholine and 5-hydroxytryptamine. 120 22

Behavioural and neurochemical effects of acute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in mice have been studied in order to determine the change in the neurotransmitter profile of the following areas of the brain: substantia nigra (SN), nucleus caudatus putamen (NCP), limbic system (LS; tuberculum olfactorium and nucleus accumbens), medulla oblongata (MO) and cerebellum (CER). Subcutaneous administration of MPTP (40 mg/kg) caused behavioural syndromes including restlessness, straub tail, hindlimb abduction, tremor, jumping, bradykinesia and akinesia in Balb/c mice. There existed a well-defined biphasic profile of motor activity comprising of an initial excitatory phase followed by an inhibitory phase lasting about two and a half and five hours, respectively. A significant rise in 5-hydroxytryptamine (5-HT) content together with a decreased 5-HT utilization as evidenced by lower 5-hydroxyindole acetic acid (5-HIAA) to 5-HT ratio in the above brain areas demarcated the excitatory phase, whereas the inhibitory phase was distinguished by a significant decrease in dopamine (DA) content along with an increased turnover of the amine as shown by a higher homovanillic acid (HVA) to DA ratio in the functionally important nuclei of the extrapyramidal system like SN, NCP and LS. Methysergide, a nonspecific 5-HT receptor blocker, but not ketanserin, a specific 5-HT2 antagonist, prevented the occurrence of the initial excitatory phase without affecting the depressive phase. Administration of apomorphine, a dopamine agonist, 30 minutes prior to MPTP was ineffective, whereas its application 90 minutes after MPTP prevented the occurrence of bradykinesia and akinesia. Interestingly, treatment with haloperidol, the dopamine (D1/D2) antagonist, before and after MPTP administration caused an early onset and prolongation of the inhibitory phase without affecting the initial hyperexcitement. The results provide direct evidence for the involvement of serotoninergic and dopaminergic mechanisms in the genesis of the early and late syndromes of acute MPTP poisoning respectively.
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PMID:Dissociation of serotoninergic and dopaminergic components in acute effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in mice. 135 Apr 96

Carbaryl (50-200 mg/kg, p.o.) produced dose-dependent tremors and inhibition of striatal AChE activity. A dose-dependent elevation of striatal 5-HT and 5-HIAA levels was also observed with carbaryl but at the higher doses (100-200 mg/kg p.o.). L-Trp or 5-HTP or haloperidol potentiated the carbaryl-induced tremors. Further, 5-HTP or haloperidol, when administered (i) alone, reduced the ED50 value and increased the duration of carbaryl-induced tremors without affecting the maximum tremorogenic response of rats and (ii) together, did not change any of these measures significantly. Atropine (acetylcholine antagonist) completely blocked the tremors produced by carbaryl in the absence or presence of 5-HTP or haloperidol. Methysergide (5-HT antagonist) and bromocriptine (DA agonist) antagonised the potentiating effect of 5-HTP and haloperidol, respectively, on the carbaryl-induced tremors. Furthermore, bromocriptine antagonised the potentiating effect of 5-HTP on the carbaryl-induced tremor but, methysergide failed to achieve this antagonism in presence of haloperidol. These results indicate that carbaryl-induced tremors primarily involve the activation of central cholinoceptors and that the serotonergic potentiation of carbaryl-induced tremors is possibly mediated through the dopaminergic disinhibition of cholinergic neurons.
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PMID:Interaction of central serotonin and dopamine in the regulation of carbaryl-induced tremor. 169 44

The administration of veratramine produced generalized tremor, myoclonus, hindlimb abduction, backward gait and Straub tail, similar to the "5-hydroxytryptamine (5-HT) syndrome", in mice. Pretreatment with metergoline, methysergide, mainserin or cyproheptadine ameliorated veratramine-induced myoclonus and tremor. For suppression of other symptoms, mianserin and cyproheptadine were effective. Metergoline improved hindlimb abduction and Straub tail, but did not inhibit backward gait. Methysergide was ineffective for the remaining symptoms. 5-Methoxy-N,N-dimethyltryptamine (5-MeODMT) enhanced all these symptoms except for Straub tail. 8-Hydroxy-2-[di-n-propylamino] tetralin hydrobromide (8-OH-DPAT) augmented tremor, hindlimb abduction and backward gait, but did not influence myoclonus and Straub tail. 5-Methoxy-3[1,2,3,6-tetrahydropyridin-4-yl] 1H-indole (RU 24969) did not modify the symptoms. Destruction of 5-HT neurons using 5,6-dihydroxytryptamine (5,6-DHT) resulted in suppression of the syndrome. The denervation supersensitivity caused by 5,6-DHT did not increase the response to veratramine. These findings indicate that part of the site of action of veratramine may be the presynaptic 5-HT neurons.
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PMID:Veratramine-induced behavior associated with serotonergic hyperfunction in mice. 171 Feb 97

LSD is the prototype for a cat behavior model for the study of hallucinogens. The model's specificity was tested with the nonhallucinogen methysergide, a d-lysergic acid amide derivative structurally similar to LSD. The frequencies of occurrence of the model behaviors limb flicking, grooming, and head plus body shaking show statistically significant dose dependency after i.p. methysergide (62.5-1000 micrograms/kg), and the maximum frequencies of the methysergide-elicited behaviors occur between 1-3 h post-dose. Methysergide produces statistically significant tolerance to limb flicking and grooming 24 h following an acute dose, and there is statistically significant methysergide-LSD and LSD-methysergide cross tolerance to limb flicking at 24 h. In addition, pretreatment with methysergide 15 min before LSD or lisuride antagonizes their elicitation of model behaviors. The dose-response, time course, and tolerance results with methysergide are analogous to those observed after LSD, showing that methysergide has all of the key properties of the model's prototype and, therefore, that the cat behavior model is not specific for hallucinogens.
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PMID:On the specificity of a cat behavior model for the study of hallucinogens. 723 73