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)

Both TRH and quipazine (2.5-25 mg/kg) were found to restore and to intensify the oxotremorine-induced tremor in mice when injected i.p. 60 min after oxotremorine 0.5 mg/kg s.c. This phenomenon does not seem to be due to an increase in body temperature or muscle tone. Also other dopaminergic drugs, e.g. amphetamine, methylphenidate, nomifensine and apomorphine had a significant but lesser effect than TRH or quipazine. Haloperidol and methysergide both antagonized the effect of quipazine but not that of TRH. Neither propranolol, phenoxybenzamine, alpha-methyl-p-tyrosine, nor p-chlorophenylalanine inhibited the activity of TRH or quipazine. The restoration of oxotremorine-induced tremor could be prevented by atropine but not by methylatropine. It is concluded that quipazine exerts its effect by direct stimulation of serotoninergic and dopaminergic receptors, whereas TRH receptors may represent separate entities and TRH may function as a neurotransmitter or neuromodulator.
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PMID:Thyrotropin releasing hormone (TRH): restoration of oxotremorine tremor in mice. Comparison with quipazine, a serotoninergic and dopaminergic stimulant. 1 78

Administration of p-chloroamphetamine (PCA) (2.5-10.0 mg/kg) or fenfluramine (FF) (5.0-15.0 mg/kg) to rats induces a behavioral syndrome--consisting of tremor, rigidity, Straub tail, hindlimb abduction, lateral head weaving and reciprocal forepaw treading--which is a reflection of the activity of central serotonin-mediated synapses. The syndrome appears within 3-5 min following i.p. administration of PCA or FF, and the syndrome-inducing effects of PCA and FF are blocked by prior depletion of serotonin with p-chlorophenylalanine. By contrast, the syndrome-inducing effect of 5-methoxy-N,N-dimethyltryptamine (5-M-DMT), which directly stimulates postsynaptic serotonin receptors, is not changed by prior serotonin depletion. Catecholamine depletion with alpha-methyl-p-tyrosine produces essentially no change in the syndrome-inducing effects of PCA, FF or 5-M-DMT. These data indicate that the initial effect of PCA or FF administration is the rapid functional release of stored serotonin.
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PMID:Behavioral evidence for the rapid release of CNS serotonin by PCA and fenfluramine. 13 Oct 36

In the rat, d-amphetamine sulfate (15--80 mg/kg) causes numerous behavioral effects including simultaneous side-to-side head weaving or head tremor, forepaw padding and splayed hindlimbs. These signs are strikingly similar to a behavioral syndrome caused by intense serotonin (5-HT) receptor activation. Experiments were designed to determine whether some of the numerous effects of amphetamine on behavior can be ascribed to actions of the drug on 5-HT mechanisms. Catecholamine depletion with alpha-methyl-p-tyrosine did not prevent the amphetamine syndrome. However, 5-HT depletion with 5,7-dihydroxytryptamine or with p-chlorophenylalanine did prevent the syndrome. The degree of syndrome inhibition by p-chlorophenylalanine was correlated with the extent of 5-HT depletion. Normal responsiveness to amphetamine in p-chlorophenylalanine-treated rats was restored by 5-hydroxytryptophan, the precursor of 5-HT. Furthermore, methysergide, a 5-HT receptor blocker, prevented the amphetamine syndrome, whereas catecholamine blockers, phenoxybenzamine and pimozide, were ineffective. The results suggest that when amphetamine causes the signs of the syndrome it does so by activating 5-HT receptors in the brain, probably by displacement of endogenous 5-HT.
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PMID:Evidence that serotonin mediates some behavioral effects of amphetamine. 30 99

The dog with an end-to-side portacaval shunt (PCS) has been extensively used as a model to investigate hepatic encephalopathy (HE) as it demonstrates a plasma amino acid pattern similar to patients with chronic liver disease. In adult mongrel dogs, the effect of PCS on plasma and CSF amino acids, octopamine (OCT), phenylethanolamine (PEA) and CSF 5-hydroxyindolacetic acid (5-HIAA), were studied. Moreover, the effect of correction of plasma amino acids by infusional techniques was investigated.Tyrosine, tryptophan and phenylalanine levels increased dramatically during the development of HE in plasma and CSF, while valine, leucine and isoleucine decreased in plasma only, but CSF levels remained stable. Plasma and CSF octopamine and phenylethanolamine and CSF 5-HIAA increased markedly as clinical features in the dogs' behavior, characteristic of hepatic encephalopathy occurred, including hypersalivation, ataxia, flapping tremor, somnolence and finally coma. Once in coma, the dogs were infused with an amino acid mixture (F080) calculated to normalize the plasma amino acid pattern. After one to eight hours, the dogs began to awake. Simultaneously, blood, and CSF aromatic amino acids returned to their control values, as did OCT, PEA and CSF 5-HIAA. If F080 infusion was stopped, biochemical alterations would appear within one week, again accompanied by clinical hepatic encephalopathy.The results indicate that the altered levels of aromatic and branched chain amino acids, octopamine and PEA in plasma and CSF correlate well with the development of HE and that correction of the plasma amino acid abnormalities improves encephalopathy simultaneously with correction of neurotransmitter derangements in CSF.
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PMID:Alterations in plasma and CSF amino acids, amines and metabolites in hepatic coma. 63 94

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

Pronounced tremors were produced in unanesthetized cats following intracaudate (I.C.) injections of either d-amphetamine (15 mug), dl-methamphetamine (20 mug), l-amphetamine (48 mug) or 3-methoxytyramine (68-120 mug). Yet, a series of other chemically and pharmacologically related phenylethylamines, including dopamine (90 mug), were not tremorogenic even at substantially higher doses. The d-amphetamine tremors developed rapidly, failed to exhibit tachyphylaxis to repeated challenging doses (15 mug) and were not influenced by pretreatment with alpha-methyl-p-tyrosine. They also developed independently of local acetylcholine activity as evidenced by the inability of cholinergic antagonists (scopolamine and hemicholinium) to interfere with the tremors. Significant qualitative differences were found between the I.C. effects of d-amphetamine (15 mug) and dopamine (15-90 mug): d-amphetamine further increased the intensity of ongoing tremors induced by physostigmine (111 mug I.C.), whereas, dopamine readily inhibited the latter. When superimposed, I.C. dopamine was equally effective in suppressing d-amphetamine tremor activity. The results emphasize the selective tremorogenic actions of d-amphetamine and call attention to the contrasting stabilizing role of dopamine. This would suggest that two types of adrenergic receptor sites are operative in the caudate in neuroregulation of involuntary movements.
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PMID:Tremorogenic effects of intracaudate d-amphetamine and their suppression by dopamine. 99 10

When human divers and experimental animals are exposed to increased environmental pressure, they develop the high pressure neurological syndrome (HPNS). Moreover, it has been recently demonstrated that pressure exposure induced an increase in striatal dopamine (DA) release. In this study, the effects of intracerebroventricular administration of a-methyl-p-tyrosine on the pressure-induced striatal DA increase, and the behavioral motor disturbances of HPNS, including hyperlocomotor activity (HLA), tremor, and myoclonia were monitored in free-moving rats. Striatal DA release was monitored by in vivo voltammetry, and behavioral symptoms using piezoelectrical sensors. Results suggested that the pressure-induced striatal DA increase could be the consequence of a release in both newly synthesized and vesicular DA. Elsewhere, data also confirmed that the pressure-induced DA disturbances would be involved in the development of HLA.
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PMID:Effects of the administration of a-methyl-p-tyrosine on the striatal dopamine increase and the behavioral motor disturbances in rats exposed to high pressure. 168 66

Mice were premedicated with reserpine and alpha-methyl-p-tyrosine to deplete stores of dopamine (DA) (and other neurotransmitters) and to stop DA (and noradrenaline (NA] synthesis. In DA-depleted mice, the mixed alpha 1/alpha 2 agonist clonidine potentiated locomotor stimulation induced by a low dose of apomorphine as measured in automated activity cages. Clonidine and the slightly alpha 1-selective agonist ST587, but not ST91, an alpha-agonist which does not readily cross the blood brain barrier, produced marked stimulation when combined with the selective D2 agonist quinpirole. The D1 -selective agonist SKF38393 also produced marked excitation when combined with quinpirole. All the selective agonists, bar quinpirole which in some cases produced a significant locomotor stimulation, were relatively inactive when given alone. A "blind" observational analysis of the animals challenged with clonidine plus quinpirole indicated an increase in sniffing, rearing and shaking behaviour. In contrast, observation of the animals challenged with SKF38393 plus quinpirole indicated increased sniffing, rearing and biting and, in one case, increased grooming behaviour. Clonidine did not produce excitation (in automated cages) when combined with the selective D1 agonist SKF38393. The excitation produced by clonidine plus quinpirole was blocked by the selective D2 antagonist raclopride but not by the selective D1 antagonist SCH23390. The stimulation was also blocked by the alpha 1 antagonist prazosin but not by the alpha 2 antagonists idazoxan or yohimbine. Biochemical analysis in the striata of mice challenged with clonidine plus quinpirole did not provide any obvious biochemical basis for the behavioural interaction. It is concluded that alpha 1 receptor agonists in combination with D2 DA agonists can produce marked stimulation in DA depleted mice.
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PMID:Alpha 1 (but not alpha 2)-adrenoceptor agonists in combination with the dopamine D2 agonist quinpirole produce locomotor stimulation in dopamine-depleted mice. 197 37

We evaluated the ability of naloxone and the mu receptor antagonist CTP (D-Phe-Cys-Tyr-D-Trp-Lys-Thr-Pen-Thr-NH2) to precipitate withdrawal in morphine-dependent mice after intrathecal (i.t.) administration. The withdrawal syndromes elicited by naloxone and CTP given i.t. were compared to those of CTP or naloxone injected intracerebroventricularly (i.c.v.). When given i.t. or i.c.v., naloxone produced the classical syndrome of events including jumping, wet dog shakes, urination, defecation followed by diarrhea, and weight loss. There was no significant difference in the potency or efficacy of naloxone when it was given i.t. or i.c.v. The profile of withdrawal effects produced by i.t. CTP resembled that caused by i.c.v. CTP; both were different from that of naloxone. The withdrawal signs seen following both i.t. or i.c.v. CTP included wet dog shakes and defecation. Mice treated with i.t. CTP lost significantly less body weight than those treated with i.c.v. CTP. In addition, i.t. and i.c.v. CTP did not stimulate jumping behaviors or diarrhea. In contrast, while i.c.v. CTP resulted in increased incidence of urination, CTP given i.t. did not. These finding indicate that naloxone given spinally acts on mu receptors to precipitate wet dog shaking and defecation, but acts on other non-mu opioid receptors (i.e. delta and/or kappa) to cause jumping, urination, diarrhea and weight loss. The differential effects of CTP given i.c.v. or i.t. suggest that supraspinal mu receptors are more involved in gastrointestinal and urinary bladder function during dependence/withdrawal than their spinal counterparts.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Precipitation of spinally mediated withdrawal signs by intrathecal administration of naloxone and the mu-receptor antagonist CTP in morphine-dependent mice. 290 Apr 67

The in vivo selectivity of the novel delta opioid-receptor antagonist N,N-bisallyl-Tyr-Gly-Gly-psi-(CH2S)-Phe-Leu-OH (ICI 154129) was examined in several opioid-selective models. Antagonism at the delta receptor was demonstrated in the striatal head-turn model in the rat. Intrapallidal injection of the relatively selective delta-receptor agonist D-Ala2,D-Leu5-enkephalin (0.5 micrograms) slowed the head-turn time and this effect was completely prevented by prior subcutaneous administration of ICI 154129 (30 mg/kg). The role of delta receptors in two classical test situations was studied using the mixed opioid agonist etorphine and the antagonists naloxone and ICI 154129. The drug ICI 154129 (30 mg/kg, s.c.) failed to prevent the antinociceptive effects and stimulation of locomotor activity produced by etorphine, whereas the relatively selective mu-opioid receptor antagonist, naloxone was effective in both test situations. The possible involvement of delta receptors in morphine-induced dependence was studied by monitoring the abstinence behaviour precipitated in rats given pellets of morphine by either ICI 154129 or naloxone. Naloxone (0.5 mg/kg, i.p.) precipitated a characteristic withdrawal syndrome in conscious rats and, at a much smaller dose (0.02 mg/kg, i.p.), induced shaking behaviour in pentobarbitone-anaesthetised rats. No withdrawal signs were observed in either model after injection of ICI 154129 (30 mg/kg, s.c.), suggesting that the delta receptors are not involved in dependence on morphine.
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PMID:In vivo evidence for the selectivity of ICI 154129 for the delta-opioid receptor. 298 29


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