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)

Oxotremorine did not alter the level of 5-HT and 5-hydroxyindoleacetic acid in different brain regions. The content of 5-HT in the striatum was diminished by electrolytic lesions of the raphe system, by microinjection of the selective depletor 5,6-dihydroxytryptamine into the raphe system and inhibition of synthesis by pCPA or pCAM. The intensity of oxotremorine-induced tremor was reduced only in some experimental groups without clear-cut correlation to the decreased 5-HT levels. In pCPA-pretreated animals resoring of 5-HT concentration by intrastriatal microinjection of 5-HT and ip administration of 5-HT did not reestablish tremor intensity. There is no evidence that cholinergic tremor is triggered indirectly and depends upon an intact 5-HT system.
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PMID:Serotonin content in the central nervous system of rats and cholinergic tremor. 12 45

Alterations of steady state and metabolism of putative neurotransmitters were studied in the brain of rats with a sustained tremor evoked by nicotine and pilocarpine. The norepinephrine content in several brain regions was decreased whereas striatal dopamine was unchanged. Homovanillic acid concentrations were slightly increased, while 5-hydroxyindoleacetic acid concentrations were markedly increased. Pilocarpine alone increased the 5-hydroxytryptamine (5-HT) turnover rate at high ambient temperature (30-32 degrees C), but not at normal ambient temperature (22 +/- 2 degrees C), atropine partially blocked the increase of 5-HT turnover rate by pilocarpine. Pretreatment with p-chlorophenylalanine and hemicholinium-3 decreased the tremor intensity elicited by nicotine and pilocarpine . It is proposed that the increase of cholinergic function caused by nicotine and the activation of muscarinic receptors and the increase in 5-HT function caused by pilocarpine might be involved in the mechanisms of tremor induction by nicotine and pilocarpine.
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PMID:Possible mechanisms of sustained tremor induction by nicotine in pilocarpine treated animals. 15 36

p-methoxyphenlethylamine (p-MPEA) induces the "serotonin syndrome" in mice which consists of lateral head weaving, Straub tail, hindlimb abduction, tremor, hyperactivity, reciprocal fore-paw treading, salivation and piloerection. These p-MPEA-induced behavioral signs were partially prevented by pretreatment with serotonin (5HT) uptake blockers (fluoxetine, chlorimipramine, Org 6582) and 5HT receptor blockers (methiothepin, methysergide, cinnanserin) but not by two depletors of brain 5HT (p-chlorophenylalanine, reserpine). p-MPEA selectively released 5HT and inhibited 5HT uptake from mouse whole brain synaptosomes. The concentrations of both 5HT and 5-hydroxyindoleacetic acid (5HIAA) in whole mouse brain were increased at 1 and 2 hours after injection of p-MPEA (50 mg/kg). The effect of p-MPEA on displacement of specific tritiated 5HT binding to membranes from mouse brain was considerably less than that of p-chlorophenylethylamine (p-CPEA), p-methoxytryptamine (pMT) and quipazine. Thus p-MPEA may induce the "serotonin syndrome" predominantly by releasing 5HT from presynaptic nerve terminals.
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PMID:Behavioral and biochemical effects of para-methoxyphenylethylamine. 46 68

A single dose of p-chloroamphetamine, 10 mg per kilogram, produced postural abnormalities, tremor, myoclonus, and autonomic signs in rats 5 minutes after intraperitoneal injection. This syndrome lasted 60 to 90 minutes, and its intensity was directly proportional to the amount of p-chloroamphetamine given over a 2 to 10 mg per kilogram range. Whole-brain levels of serotonin and 5-hydroxyindoleacetic acid were not altered during this interval, although both were reduced significantly 1 day later. Pretreatment with drugs that interfere with the uptake of p-chloroamphetamine into terminals of serotonergic neurons (fluoxetine), depress brain serotonin levels (p-chlorophenylalanine), or block serotonin receptors (methiothepin or methergoline) suppressed this syndrome, whereas drugs that antagonize the effects of dopamine, norepinephrine, and acetylcholine did not. These observations implicate serotonergic mechanisms and provide behavioral evidence of p-chloroamphetamine's immediate actions on serotonergic neurons in the central nervous system.
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PMID:Postural changes, tremor, and myoclonus in the rat immediately following injections of p-chloromaphetamine. 56 3

The effect of the estrogen-like chlorinated pesticide chlordecone (Kepone) on sexual behavior was examined in proestrous rats following treatment with 25, 50, or 75 mg/kg chlordecone. In most animals, sexual behavior, both receptivity and proceptivity, was reduced within 60 min following the higher dosage of chlordecone. Reduced sexual receptivity occurred more slowly with 50 mg/kg chlordecone (usually within 180 min) and no reduction was seen following 25 mg/kg chlordecone. The reduced sexual behavior after chlordecone treatment preceded the onset of marked chlordecone-induced tremor. A group of rats treated with 75 mg/kg chlordecone was euthanized at the time that behavioral inhibition began to develop. The content of serotonin, norepinephrine, and their principal metabolites was determined by high-performance liquid chromatography of extracts of brain tissue of these animals. In hypothalamus, increases in serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) content, and a decrease in the level of norepinephrine (NE), were detected in chlordecone-treated rats relative to matched controls which received vehicle. The content of 5-HT was also increased in preoptic area of chlordecone-treated females. The content of the catecholamine metabolite, 3,4-dihydroxy-phenylacetic acid, was unaffected by chlordecone in either part of brain. These are the first observations of the parallel effects of chlordecone on receptive and proceptive behaviors, and on neurochemistry, in female rats; the results demonstrate short-latency effects of the pesticide treatment on the CNS events that mediate female reproductive behavior. Results of previous studies had led to the suggestion that chlordecone's inhibition of sexual behaviors resulted from its interaction with the intracellular estrogen receptor. However, the rapidity of the inhibition during the period of ongoing sexual behavior makes it unlikely that the inhibition is mediated by the pesticide's action at the intracellular estrogen receptor. Because of the importance of sexual behaviors to reproductive fitness, the current results indicate that nonsteroidal, behavioral mechanisms could contribute to chlordecone's neuroreproductive toxicity.
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PMID:Chlordecone (Kepone) on the night of proestrus inhibits female sexual behavior in CDF-344 rats. 171 37

Rats were given 75 mg/kg of 5,5-diphenylhydantoin (phenytoin) or vehicle 30 min prior to 75 mg/kg of 1,1,1-trichloro-bis(p-chlorophenyl)ethane (p,p'-DDT) (p.o.) or chlordecone (i.p.) and tremor was measured 12 h later. Rats were then killed, and regional brain levels of biogenic amines and their acid metabolites and amino acids were determined. Pretreatment with phenytoin significantly attenuated the tremor produced by p,p'-DDT but enhanced that produced by chlordecone. p,p'-DDT had significant effects on the levels of aspartate, glutamate, 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG), whereas chlordecone increased glycine, 5-HIAA, and MHPG levels. Pretreatment with phenytoin blocked p,p'-DDT-induced increases of aspartate in the brainstem and spinal cord, 5-HIAA in the hippocampus, and MHPG in the brainstem and hypothalamus. Phenytoin significantly enhanced chlordecone-induced increases of MHPG in the brainstem. These data indicate that organochlorine-induced increases in noradrenergic activity in the brainstem and spinal cord may be directly related to the tremorigenic effects of these chemicals.
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PMID:5,5-Diphenylhydantoin antagonizes neurochemical and behavioral effects of p,p'-DDT but not of chlordecone. 243 63

LON-954 [N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride], a novel tremorogen known to affect the central dopaminergic system, has been investigated in rats for tremor and 5-hydroxytryptamine (5-HT) metabolism. Five, 10 and 20 mg/kg of LON-954 IP caused a reproducible and consistent tremor with a high frequency (16 Hz) within 2 minutes and lasting 30-45 minutes. 5-HT content of the tuberculum olfactorium and basal ganglia was found to be increased significantly at a time when 5-hydroxyindoleacetic acid (5-HIAA) content showed a decrease. 5-HT and 5-HIAA of medulla oblongata showed significant changes only after 15 minutes. The alterations in the levels of the indoleamine in tuberculum olfactorium and its relationship with dosage as well as duration and intensity of LON-954 tremor indicate the involvement of the mesolimbic system in its action. A direct role of 5-HT in LON-tremor was evidenced since the drug failed to produce tremor in rats pretreated with p-chlorophenylalanine (300 mg/kg IP) for 3 days.
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PMID:Tremorogenesis by LON-954 [N-carbamoyl-2-(2,6-dichlorophenyl) acetamidine hydrochloride]: evidence for the involvement of 5-hydroxytryptamine. 270 33

Male, Fischer strain 344 adult rats were given various doses (25-100 mg/kg) of p,p'-DDT by oral gavage, and levels of biogenic amines, their metabolites, and amino acid neurotransmitters, tremor activity, and rectal temperature were measured at several intervals (2, 5, 12, and 24 h) after dosing. Dose-related increases in rectal temperature and in tremor activity were observed at 50-100 mg/kg 12 h after dosing. Tremorigenic doses of DDT increased the 5-hydroxyindoleacetic acid (5-HIAA) level in hypothalamus, brainstem, and striatum, whereas doses of 75 and 100 mg/kg increased the 3-methoxy-4-hydroxyphenylglycol (MHPG) level in hypothalamus and brainstem and the 3,4-dihydroxyphenylacetic acid level in striatum. Six amino acids were assayed in the brainstem, hypothalamus, and striatum; aspartate and glutamate levels were increased only in brainstem at 25-100 mg/kg. No consistent changes in concentrations of taurine, glutamine, glycine, or gamma-aminobutyric acid were observed in any of the regions assayed. Time-related increases in rectal temperature were seen 2-12 h after dosing, and the presence of tremor was observed 5-12 h after dosing; for both the time of peak effect was at 12 h. The DDT-induced hyperthermia and tremor were associated with dose- and time-related increases in levels of 5-HIAA, MHPG, aspartate, and glutamate. It is suggested that an increase in the turnover rate of 5-hydroxytryptamine (5-HT) may be responsible for the DDT-induced hyperthermia, whereas increases in the metabolism of 5-HT and norepinephrine may be involved in the tremor.
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PMID:Effects of p,p'-DDT on the rat brain concentrations of biogenic amine and amino acid neurotransmitters and their association with p,p'-DDT-induced tremor and hyperthermia. 286 92

Our previous data demonstrated that both 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium ion (MPP+) exerted potent inhibition on endogenous 3,4-dihydroxyphenylacetic acid (DOPAC) output and potent stimulation on endogenous dopamine (DA) release from the rat corpus striatum superfused in vitro. In this report, using a push-pull perfusion technique, we examined in vivo the acute effects of MPTP and MPP+ on DA metabolism in the rat caudate nucleus (CN). MPTP or MPP+ in modified Krebs-Ringer phosphate buffer at concentrations of 10(-6), 10(-5) and 10(-4) M was administered directly into the CN for 15 min, each 90 min apart. Thirty minutes after the infusion of 10(-6) M MPP+, DOPAC output was reduced to a significantly lower value and subsequent infusions of high concentrations of MPP+ further decreased DOPAC output. Homovanillic acid (HVA) output was also decreased by MPP+ infusions, however, at higher concentrations. In respect to DA release, 1 of 10, 4 of 10 and 7 of 10 animals responded with significant increases to 10(-6), 10(-5) and 10(-4) M MPP+, respectively. On the other hand, MPTP was effective in reducing DOPAC output only at 10(-4) M and ineffective in altering DA and HVA output at all doses tested. In addition, neither drugs had a significant effect on 5-hydroxyindoleacetic acid. Accompanying the dramatic changes in DA metabolism caused by MPP+, two uncommon behavioral syndromes were also observed; tremor-body twist and body shaking.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects on dopamine metabolism of MPTP and MPP+ infused through a push-pull cannula into the caudate nucleus of awake adult male rats. 331 41

Mean homovanillic acid and 5-hydroxyindoleacetic acid concentrations were significantly low in the lumbar CSF of a group of patients with disseminated sclerosis (DS) who were severely disabled but not in the CSF of a less severely restricted group with DS. CSF concentrations were also low in a group of patients with superior cerebellar peduncular tremor due to DS and in a single patient with a similar tremor associated with a post-traumatic brain-stem lesion. The interpretation of abnormal CSF amine metabolite concentrations is discussed in the light of these findings.
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PMID:Amine metabolites in the cerebrospinal fluid of patients with disseminated sclerosis. 484 38


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