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)

Treatment of common marmosets with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 1-4 mg/kg for up to 4 days) caused a profound parkinsonian state. Ten days from the start of MPTP treatment, all animals showed marked motor impairment, consisting of bradykinesia and akinesia, limb rigidity, postural abnormalities, loss of vocalisation and blink reflex, and, on occasions, postural tremor. Measurement of caudate-putamen monoamine content at this time showed a profound loss in 3,4-dihydroxyphenylethylamine, homovanillic acid, and 3,4-dihydroxyphenylacetic acid concentrations. Measurement of neuropeptide concentrations in the caudate-putamen, internal and external segments of the globus pallidus, nucleus accumbens, substantia nigra, frontal cortex, and hippocampus showed met-enkephalin, leu-enkephalin, and cholecystokinin (CCK-8) concentrations to be unaffected by MPTP treatment. There was a small decrease in the substance P content of frontal cortex, but otherwise the content of this neuropeptide was unaltered. Parkinsonism in the marmoset, induced by MPTP treatment 10 days earlier, does not alter neuropeptide concentrations in the manner observed in Parkinson's disease.
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PMID:Lack of change in basal ganglia neuropeptide content following subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment of the common marmoset. 242 37

The behavioral and biochemical effects of intracerebroventricular administration of cholecystokinin were investigated in experiments on male Wistar rats. Cholecystokinin induced specific dose-dependent changes in the behavior of the animals. At low doses the inhibiting influence on behavior predominated; at high doses stereo-typed behavior, shaking of the head and increased reactivity to pain stimuli were observed. Cholecystokinin appreciably inhibited the circulation of serotonin and dopamine in the brain structures in comparison with physiological saline solution. Administration of cholecystokinin against a background of phenamine and 5-hydroxy-tryptophan briefly entirely inhibited the behavioral effects induced by these substances. On the basis of the data obtained it can be assumed that cholecystokinin is an endogenous modulator of the activity of the monoaminergic systems of the brain.
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PMID:Intracerebroventricular administration of cholecystokinin inhibits the activity of the dopaminergic and serotoninergic systems of the brain. 299 47

The anticonvulsive activity of cholecystokinin octapeptide sulphate ester (CCK-8-SE), non-sulphated cholecystokinin octapeptide (CCK-8-NS) and three different N- and C-terminal fragments were investigated against seizures induced by picrotoxin and electroshock in rats after intracerebroventricular administration. Doses of 0.8 and 80 pmol of CCK-8-SE and CCK-8-NS significantly enhanced the latency of seizures induced by picrotoxin and shortened the duration of the clonic phase of the seizures induced by electroshock. Only CCK-8-SE shortened the recovery time and only 0.8 pmol of CCK-8-SE could shorten the duration of the tonic phase of convulsions induced by electroshock. Doses of the octapeptides of 8000 pmol were ineffective, with the exception of CCK-8-NS in the picrotoxin test. Of the fragments tested, the C-terminal tetrapeptide, CCK-5-8, enhanced the latency of seizures induced by picrotoxin in a dose of 0.8 pmol, and had a dose-dependent biphasic effect on the duration of the clonic phase of seizures induced by electroshock. Intracerebroventricular administration of diazepam enhanced only the latency of tremor and clonic seizures induced with picrotoxin in a dose of 40 nmol. Twelve nmole of diazepam shortened the clonic phase of convulsions induced by electroshock. The peptides tested were much more active than diazepam, and their effective doses were comparable to the amounts of cholecystokinin octapeptide found in brain structures.
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PMID:Inhibition of seizures induced by picrotoxin and electroshock by cholecystokinin octapeptides and their fragments in rats after intracerebroventricular administration. 609 Sep 68

Intracerebroventricular (i.c.v.) injection of C-terminal octapeptide of cholecystokinin (CCK-8) in rats prolonged pentobarbital- and ethanol-induced sleeping time, but non-sulfated CCD-8 (CCK-8-NS) had no effect and caerulein showed a tendency to prolong the pentobarbital narcosis. On the other hand, i.c.v. injection of thyrotropin releasing hormone (TRH) shortened the sleeping time and the effect of CCK-8 was apparently antagonized by combined administration of TRH. Spontaneous locomotor activity in the late morning and early afternoon was not affected by CCK-8, but it increased following i.c.v. injection of CCK-8-NS. Hyperactivity produced by TRH and methamphetamine was suppressed by i.c.v. injection of CCK-8, while CCK-8-NS showed a tendency to enhance the methamphetamine-induced hyperactivity and caerulein had no effect. These results indicate that CCK-8 has a sedative action and antagonizes the behavioral excitation caused by TRH and methamphetamine, but that the effects of CCK-8-NS and caerulein were rather the opposite of those of CCK-8. In an additional experiment the TRH-induced body shaking response was not affected by combined administration of CCK-8.
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PMID:Sedative action of cholecystokinin octapeptide on behavioral excitation by thyrotropin releasing hormone and methamphetamine in the rat. 628 7

Effects of intracerebroventricular administration of beta-endorphin, thyrotropin-releasing hormone (TRH), cholecystokinin octapeptide (CCK-8), non-sulfated CCK-8 (CCK-8-NS) and caerulein on body shaking behavior were observed in rats. CCK-8 and its related peptides produced only a small increase in the number of body shakes, while TRH had the striking effect of stimulating body shakes, this increase being markedly suppressed by simultaneous administration of beta-endorphin. Moreover, the suppressive effect of beta-endorphin on TRH-induced body shakes was antagonized by simultaneous administration of caerulein and CCK-8. The body shakes induced by ice-water immersion were also reduced by beta-endorphin, this beta-endorphin effect being partly antagonized by caerulein and CCK-8.
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PMID:Effects of beta-endorphin, thyrotropin-releasing hormone and cholecystokinin on body shaking behavior in rats. 629 91

Interaction of cholecystokinin (CCK) with vasoactive intestinal peptide (VIP) in body shaking response to ice-water immersion was observed in pentobarbital-anesthetized rats. Although CCK itself had no influence on the response, VIP suppressed it and this effect of VIP was antagonized by simultaneous administration of sulfated octapeptide of CCK, but not by non-sulfated CCK.
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PMID:Interaction of cholecystokinin with vasoactive intestinal peptide in body shaking response to ice-water immersion in rats. 664 3

Recently, cholecystokinin (CCK) has been reported to antagonize a variety of opiate-induced effects, including nociception, body shaking, thermoregulation, and locomotion. Consistent with these results, a number of CCK antagonists potentiate the opiates in a range of behavioral and physiological assessments. The present study further examined the interaction between CCK and the opiates within the conditioned taste aversion baseline of drug discrimination learning, a design that utilizes the stimulus properties of the drug to control consummatory behavior. Specifically, animals injected with CCK prior to saccharin-LiCl pairings and the CCK vehicle prior to saccharin alone rapidly acquired the CCK-vehicle discrimination, avoiding saccharin consumption following the administration of CCK and consuming the same saccharin solution following the vehicle. Although the stimulus properties of CCK did not generalize to either naloxone or diprenorphine, morphine blocked and naloxone potentiated CCK's stimulus effects. These data are thus consistent with a physiological (rather than a pharmacological) interaction between CCK and the opiates.
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PMID:An assessment of the interaction between cholecystokinin and the opiates within a drug discrimination procedure. 825 17

N-Methyl-D-aspartate (NMDA, 20 mg/kg) produced a clear decrease in mouse exploration in open parts of an elevated plus-maze. Paradoxically, 40 mg/kg NMDA did not modify the behavior of the mice in the plus-maze. NMDA at a dose of 80 mg/kg again depressed the exploratory activity of mice, but this effect was accompanied with tremor and compulsive tail biting. The 'anti-exploratory' dose of NMDA (20 mg/kg) increased, whereas the 'tremorigenic' dose (80 mg/kg) significantly decreased the number of cholecystokinin (CCK) binding sites in the mouse cerebral cortex. The competitive NMDA antagonist (+/-)-CPP (2.5-5 mg/kg) and the non-competitive antagonist MK-801 (0.25 mg/kg) antagonized the anti-exploratory effect of NMDA (20 mg/kg). The tricyclic antidepressant imipramine (5 mg/kg, but not 1 or 10 mg/kg) also attenuated the inhibition of exploratory activity induced by NMDA. Of three CCK receptor antagonists tested, the unselective CCK antagonist proglumide (1 mg/kg, but not 0.1 and 10 mg/kg) significantly opposed the anti-exploratory action of NMDA. The selective CCK antagonists L-365,260 (1 microgram/kg) and devazepide (1 microgram/kg) were evidently weaker antagonists of NMDA. Furthermore, 10 micrograms/kg of L-365,260, a CCK-B receptor antagonist, and 1 mg/kg of devazepide, a CCK-A receptor antagonist, even tended to augment the effect of NMDA in the plus-maze. The results of the present study seem to give some support to the notion that not only NMDA receptors, but also CCK-ergic mechanisms are involved in the modulation of anti-exploratory action of NMDA in the elevated plus-maze.
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PMID:Anti-exploratory effect of N-methyl-D-aspartate in elevated plus-maze. Involvement of NMDA and CCK receptors. 847 31

Two men, aged 63 and 71 years, developed a gross action tremor and dysesthesias several months after an intracerebral hemorrhage. CT and MRI showed a small hemorrhage in the posterior region of the lateral nucleus of the thalamus in each patient. The tremor occurred on movement, had frequencies of 2.5-4.5 Hz and the amplitude varied depending on the joint position of the limb. Ceruletide (a cholecystokinin analog) 0.8 micrograms/kg i.m. produced a marked reduction in the action tremor and improved motor function. This effect appeared 10-15 min after the injection, and lasted for up to 4 weeks. It is suggested that ceruletide may be of value in the treatment of action tremors following a thalamic lesion.
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PMID:Ceruletide therapy in action tremor following thalamic hemorrhage. 848 85