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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Effect of 3, 4-dihydroxyphenylserine (DOPS), a norepinephrine precurosr, on harmaline tremor was investigated in mice to elucidate the role of norepinephrine in the genesis of tremor. 1) Spontaneous motor activity was inhibited by L-threo-DOPS (200 mg/kg i.p.). 2) Tremor induced by harmaline (5 and 7 mg/kg i.p.) was enhanced by alpha-methyl-p-tyrosone (200 mg/kg i.p.). 3) The development and duration of tremor induced by harmaline (10 mg/kg i.p.) were inhibited significantly in a dose dependent manner by L-threo-DOPS (50, 70, 100, 150 and 200 mg/kg i.p.), but neither by D-threo-DOPS (200 mg/kg i.p.) nor DL-erythro-DOPS (200 mg/kg i.p.). 4) L-threo-DOPS (200 mg/kg i.-.) had no effect on the development of tremor induced by tremorine (5 and 10 mg/kg i.p.), while lacrimation and diarrhea caused by tremorine was markedly inhibited. 5) Administration of harmaline (10 mg/kg i.p.) produced an increase in brain 5-hydroxytryptamine content but not in that of norepinephrine. Administration of L-threo-DOPS (100 mg/kg i.p.) increased the norepinephrine content but not the 5-hydroxytryptamine content in the brain. Inhibition of harmaline tremor induced by L-threo-DOPS is attributed to the L-norepinephrine converted from L-threo-DOPS and the involvement of a noradrenergic mechanism in harmaline tremor has to be considered.
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PMID:[Inhibition of harmaline induced tremor by L-threo-3, 4-dihydroxyphenylserine, an L-norepinephrine precursor]. 98 92

1. The effect of various agents injected into the cerebral ventricles of the mouse, upon the tremor and hypothermia produced by oxotremorine (0.5 mg/kg i.p.) was studied. 2. Acetylcholine (0.1-10 mug) produced a dose-dependent potentiation of oxotremorine tremor in contrast to the multiphasic effect it had on the accompanying hypothermia. Both tremor and hypothermia were antagonised by very small doses (0.1-10 ng) of atropine. 3. Dopamine and apomorphine (0.1-10 mug) had no significant effect on oxotremorine tremor. A dose-dependent potentiation of hypothermia was, however, observed. 4. Noradrenaline (0.1-10 mug), phentolamine and propranolol (0.1-10 mug) produced no significant effect on tremor and inconsistent results were obtained on hypothermia. 5. Neither tremor nor hypothermia were affected by 5-hydroxytryptamine (1-20 mug). 6. Oxotremorine tremor appears to be due solely to the activation of cholinergic pathways, whereas the production of hypothermia is brought about via a system involving both cholinergic and dopaminergic components. 5-Hydroxytryptamine is not involved.
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PMID:Modification of oxotremorine tremor and hypothermia by injections of drugs into the cerebral ventricles of the mouse. 101 35

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

The brain lesion technique was used to destroy the ascending 5-hydroxytryptamine (5-HT) system at its cell bodies in the dorsal and medial raphe nuclei in order to assess the importance of 5-HT for the induction of harmine tremor and its antagonism by the dopaminergic agonists, L-DOPA, apomorphine and d-amphetamine. Lesions of the medial or dorsal raphe nucleus reduced the intensity of harmine tremor. The remaining tremor was generally resistant to further reduction by the dopaminergic agonists. 5-hydroxytryptophan was shown to enhance tremor: this effect was reduced both by the raphe lesions and by treatment with L-DOPA. The data are discussed in terms of the possible relationship between 5-HT and dopamine.
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PMID:The importance of 5-hydroxytryptamine for the induction of harmine tremor and its antagonism by dopaminergic agonists assessed by lesions of the midbrain raphe nuclei. 125 13

There is both experimental and clinical evidence to suggest a role for 5-hydroxytryptamine (5-HT) in Parkinson's disease. The effect of ritanserin, a highly selective 5-HT2 receptor antagonist, on Parkinsonian symptomatology was investigated in 10 patients in a single-blind placebo-controlled study. Akinesia and gait improved significantly in a dose-dependent manner in 5 and 7 patients respectively. However there was no significant improvement in tremor. The effects of ritanserin on akinesia and gait are consistent with a role for 5-HT in Parkinson's disease.
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PMID:Effect of ritanserin, a highly selective 5-HT2 receptor antagonist, on Parkinson's disease. 134 70

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

The behaviors induced by the 5-hydroxytryptamine (5-HT) precursor 5-hydroxytryptophan (5-HTP) has been called the "5-HT (serotonin) syndrome." These behaviors and others identified in rat pups were observed following administration of 5-HTP (300 mg/kg, SC) on postnatal (PN) days 3, 14, and 28 and in adult rats. Certain 5-HT syndrome behaviors and other uniquely neonatal behaviors were present in PN3 pups treated with vehicle. 5-HTP-treated PN3 pups showed increased head-shakes, rollovers, vocalizations, and forepaw treading and decreased hindlimb abduction. No 5-HT syndrome or neonatal behaviors were present at PN14 or PN28 or in adults treated with vehicle. 5-HTP administered at PN14 stimulated circling, forepaw treading, and resting tremor; at PN28, stimulated head-shakes and resting tremor; and in adults produced only head-shakes. To determine if prior exposure to 5-HTP affected the sensitivity of 5-HT receptor subtypes, the 5-HT1A agonist (+/-)-8-hydroxy-dipropylaminotetralin (8-OH-DPAT) and the 5-HT2/1C agonist (+/-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (DOI) were administered to all rats as adults. 8-OH-DPAT (1 mg/kg, SC) produced flattened body posture unaffected by prior exposure to 5-HTP. Head-shakes induced by DOI (5mg/kg, IP) were decreased by prior exposure to 5-HTP at PN3 and adult, but increased by preexposure at PN28. Thus, serotonergic neural systems are implicated in some behaviors of neonates. The developmental patterns suggest changes in the sensitivity to these systems. Further, lasting changes in 5-HT2/1C receptor sensitivity occur due to exposure to 5-HTP.
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PMID:Behaviors induced by 5-hydroxytryptophan in neonatal, preweaning, postweaning, and adult Sprague-Dawley rats. 140 74

Although numerous subtypes of serotonin [5-hydroxytryptamine (5-HT)] receptors have been identified in the newborn rat by radioligand binding studies, there have been few studies of the functional significance of these early receptors, most without the benefit of selective drugs. We performed acute dose-response and time course behavioral studies in 1-day-old rats with the putative selective agonists 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) (5-HT1A), 5-methoxy-3(1,2,3,6-tetrahydropyridin-4-yl)1H-indole (RU 24969) (5-HT1B), and (+-)1-(2,5-dimethoxy-4-iodo-phenyl aminopropane)-2 (DOI) (5-HT2/1C). The agonists induced distinctive behavioral syndromes. The DOI syndrome mainly included rudiments of forepaw myoclonus and dystonic limb postures, but no shaking behavior (head shakes or wet-dog shakes) or spinal myoclonus, two key reference behaviors for its effects in adult rats. The most distinctive feature of the 8-OH-DPAT-induced syndrome was flat body posture. RU 24969 most significantly increased locomotor activity, inducing propulsive movements with episodic rests and sudden hindlimb jerks. These studies suggest that functional and differential activity of 5-HT1A, 5-HT1B, and 5-HT2/1C receptors occurs much earlier in the rat than previously appreciated. The absence of DOI-induced shaking behavior and spinal myoclonus, however, suggests incomplete maturation at the level of the receptor or effector pathways for these behaviors.
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PMID:Serotonin receptor ontogeny: effects of agonists in 1-day-old rats. 147 12

The role of the amygdaloid complex in the central regulation of the cardiovascular system was studied in unanesthetized, unrestrained rat. The injection of carbachol into the amygdaloid complex elicited a pressor response, whereas the injection of noradrenaline and 5-hydroxytryptamine into the same area caused no significant cardiovascular changes. The greatest pressor response was obtained when carbachol was injected into the central nucleus. Bradycardia and tachycardia occurred when injection of carbachol was made into dorso-central and medio-ventral parts of the amygdaloid complex, respectively. Concomitant with cardiovascular responses, the injection of carbachol into the amygdaloid complex produced behavioral changes including immobilization, body shaking, searching and rearing. The pressor response and bradycardia were suppressed by prior local injection into the amygdaloid complex of atropine but not hexamethonium. These results suggest that the cholinergic system mediated by activation of muscarinic receptors in the amygdaloid complex may play a role in the control of cardiovascular and autonomic function.
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PMID:Cardiovascular changes induced by chemical stimulation of the amygdala in rats. 167 6


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