Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027066 (myoclonus)
 4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Differential effects of neuropharmacological drugs upon susceptibility to flurothyl-induced myoclonic and clonic convulsions were assessed in two selectively bred lines of mice. Dopaminergic drugs (apomorphine and haloperidol) only affected myoclonus, whereas cholinergic (pilocarpine and scopolamine), gabaergic (AOAA and bicuculline), and serotonergic (PCPA) compounds principally influenced clonus. Noradrenergic drugs (clonidine, phentolamine and sotalol), however, altered the expression of both types of seizures. The apparent differential neurohumoral modulation of myoclonus and clonus is discussed in light of previous suggestions that these behaviors have separate neural substrates.
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PMID:Differential neurohumoral modulation of myoclonic and clonic seizures. 3 68

The effects of four neural excitants (damphetamine, cocaine, nicotine, and strychnine) on myoclonic and clonic seizure susceptibility were investigated in two age groups (30 and 120 days) of short-sleep mice. Amphetamine and cocaine decreased susceptibility to myoclonus in young mice and increased susceptibility in mature mice. These effects were attenuated by pretreatment with haloperidol, indicating mediation by a dopaminergic system. Amphetamine did not alter clonic susceptibility in either age group of mice, whereas cocaine affected clonic susceptibility and myoclonus. These effects were not attenuated by haloperidol, indicating mediation by systems other than dopamine. Nicotine decreased susceptibility to myoclonus and increased susceptibility to clonus, whereas strychnine increased susceptibility to both types of seizure. Haloperidol, however, failed to alter any of these effects. These results are consistent with our previous work which suggests that a dopaminergic mechanism in these mice undergoes marked developmental changes between 30 and 120 days of age.
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PMID:Maturational changes related to dopamine in the effects of d-amphetamine, cocaine, nicotine, and strychnine on seizure susceptibility. 11 67

The dose-related time course and occurrence of different seizure subtypes was examined in mice after i.c.v. administration of N-methyl-D-aspartate (NMDA), kainate (KA) or quisqualate (QA). At doses of 0.2 to 1 nmol, NMDA dose-dependently induced a single clonic-tonic seizure. Low doses (0.1 to 0.3 nmol) of KA induced only mild myoclonus and whole body clonus, which were dose-dependently replaced by short-delay clonic-tonic seizures at higher doses (0.4 to 1.2 nmol). In contrast, mice treated with 13 to 32 nmol of QA exhibited either mild myoclonus or whole body clonus as well as clonic-tonic seizures. Clonic-tonic seizures induced by NMDA or KA appeared at shorter latencies than those induced by QA, whereas whole body clonus induced by KA or QA appeared with long onset latencies. These results clearly show that i.c.v. administration of NMDA, KA and QA produces different patterns of seizures in mice. This study confirms that NMDA, KA and QA induce convulsions through different underlying mechanisms and suggests that different anatomical pathways are involved in these models.
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PMID:Comparative analysis of seizures induced by intracerebroventricular administration of NMDA, kainate and quisqualate in mice. 157 1

Immediately after a patient with myoclonus epilepsy smoked a nicotine-containing cigarette, tetraparesis and hyperreflexia with ankle clonus developed, but disappeared within several minutes. During paresis, the H-reflex size of the soleus muscle increased, EEG showed more slow waves than before smoking, and the cerebral perfusion increased around the motor cortex as shown by single photon emission CT. A similar effect occurred when the patient chewed nicotine gum, and smoking a cigarette with a high nicotine content induced severe positive and negative myoclonus after the development of tetraparesis. Administration of the C6-type nicotinic antagonist mecamylamine not only countered the smoking effect, but ameliorated the spontaneous positive and negative myoclonus. Mecamylamine may prove useful for the treatment of positive and negative myoclonus in myoclonus epilepsy.
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PMID:Nicotine-sensitive paresis. 173 70

Abecarnil (ZK 112119; isopropyl-6-benzyloxy-4-methoxymethyl-beta-carboxylate) is a metabolically stable beta-carboline derivative with potent anxiolytic and few sedative and ataxic effects in rodents. The anticonvulsant and muscle relaxant actions of abecarnil have been evaluated in mice, rats, gerbils and baboons. Abecarnil raised the threshold for tonic electroconvulsions in mice after corneal but not after auricular application, had no effect on maximal electroshock-induced tonic convulsions triggered by either method, protected mice against the tonic hindlimb extension in PTZ-, picrotoxin- and 3-mercaptopropionate-induced seizures and blocked clonus after PTZ, DMCM (methyl-4-ethyl-6,7-dimethoxy-9H-pyrido-(3,4-b)-indol-3-carboxylate) and 3-mercaptopropionate. Abecarnil had no effect on convulsions induced by bicuculline and strychnine. Furthermore, abecarnil blocked kindled seizures after chronic administration of PTZ and FG 7142 (beta-carboline-3-carboxylic acid methylamide) and protected mice and rats against limbic convulsions induced by pilocarpine. Severity and afterdischarge duration of amygdala-kindled seizures were reduced in rats treated with abecarnil. Abecarnil also antagonized selectively convulsions induced by i.c.v. administration of kainate, but not those triggered by N-methyl-D-aspartate or quisqualate. In genetic models of reflex epilepsy, abecarnil was effective against sound-induced convulsions in DBA/2 mice, against air blast-induced generalized seizures in gerbils and against myoclonus in baboons Papio papio. The anticonvulsant effect of abecornil in a PTZ seizure model in mice was potentiated by ethosuximide, whereas no significant potentiation was found with diazepam, clonazepam, diphenylhydantoin, carbamazepine and phenobarbital. Electromyographic monitoring in a etorphine model of muscle rigidity in rats showed no or little muscle relaxant effect of abecarnil.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Anticonvulsant action of the beta-carboline abecarnil: studies in rodents and baboon, Papio papio. 197 Mar 62

Myoclonus is a clinical term meaning a quick involuntary jerk, seen in normal subjects under certain circumstances, including sleep, and in certain disease states. It is important as a symptom that may impair function and as an indicator of neurological dysfunction. Not until patients with myoclonus and major functional disability were reported in the 1960s was attention given to understanding its basis and pharmacotherapy. Reports of myoclonus developing after anoxic brain injury, and its response to treatment with the serotonin precursor 5-hydroxytryptophan (5-HTP), drew special attention. Further experience showed that only a few patients with myoclonus benefit from 5-HTP therapy. Benzodiazepines (BDZs) are often helpful in the treatment of myoclonus. Their beneficial effects decline with chronic administration because of drug tolerance, and the theoretical basis for BDZ responses remains unclear. The relationships between myoclonus, clonus, and epilepsy are discussed, as is the possible contribution of slow signaling transmembrane receptors to synchronization of motoneuron firing, which is suggested as a hallmark of myoclonus. Myoclonus may originate in many CNS sites, but the brain-stem reticular formation is especially relevant to myoclonus. Brain-stem serotonin neurons have special influence on spinal motoneurons, on startle responses, and on myoclonus. Among 5-HT receptors, 5-HT1A receptors are related to some forms of myoclonus, although 5-HT2 receptors are also implicated. GABAA receptors are related to some forms of myoclonus. Blockade of GABAA receptors or GABA synthesis regularly evokes convulsive seizures, but administration of many GABA agonists and some GABA uptake blockers paradoxically may evoke myoclonus. Injection of GABA receptor blockers into some brain areas has anticonvulsant effects. Stimulation of GABAA receptors may therefore promote or antagonize myoclonus depending on which GABA receptors are involved, the state of the system, etc. The role of glycine receptors is well established in some animal models, but has yet to be clearly established for human myoclonus. Opiates may produce myoclonus when given intrathecally or in high dosage. The concept of excitant anesthetics and special function of certain GABA receptors is discussed.
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PMID:Myoclonus: analysis of monoamine, GABA, and other systems. 216 12

It has been hypothesized that the Long-Sleep and Short-Sleep mouse lines were bidirectionally selected for high and low brain excitability, and further, that these differences are mediated by the benzodiazepine/gamma-aminobutyric acid (GABA) receptor-chloride channel complex. Hence, mice from both lines were administered seven convulsants (bicuculline, pentylenetetrazol, 3-carbomethoxy-beta-carboline, picrotoxin, caffeine, flurothyl and strychnine) and myoclonic and clonic seizure latencies recorded. Supporting the original hypothesis, the results show that the two lines were differentiated by all of the convulsants and that in response to the drugs, three distinct convulsive patterns were found. Nevertheless, a simple genetic model accounting for these results was not evident. To further clarify these susceptibility patterns, a convulsant representing each of these patterns (bicuculline, pentylenetetrazol or caffeine) was administered in conjunction with the anticonvulsant-barbiturate phenobarbital or the benzodiazepine antagonist Ro 15-1788. Irrespective of the convulsant given, phenobarbital attenuated both myoclonus and clonus subsequent to all convulsants, while Ro 15-1788 had a more discrete anticonvulsant profile.
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PMID:Patterns of convulsive susceptibility in the long-sleep and short-sleep selected mouse lines. 250 42

The convulsant potency of bicuculline, a GABA antagonist, was shown to be greater in Short-Sleep (SS) mice than in Long-Sleep (LS) mice. LS mice, selectively bred for lengthy ethanol-induced narcosis, had longer latencies to myoclonus and clonus following administration of bicuculline and picrotoxin than did ethanol-resistant SS mice. SS mice were also more susceptible to pentylenetetrazol-induced myoclonus, but not clonus. F1 hybrids showed bicuculline seizure sensitivity intermediate to the two parent lines. Ethanol weakly inhibited bicuculline-induced myoclonus in both LS and SS mice. Clonus was clearly antagonized by ethanol in both lines, but to a similar degree. These data provide evidence for a GABAergic role in genotype-dependent sensitivity to ethanol.
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PMID:Convulsant properties of GABA antagonists and anticonvulsant properties of ethanol in selectively bred long- and short-sleep mice. 250 97

Bovine spongiform encephalopathy (BSE) was diagnosed in a cow with a history of behavioral change, apprehension, hyperesthesia to auditory and tactile stimuli, wide-based stance, and marked hind limb hypermetria. Myoclonus involving individual muscles was observed in the shoulder region, ventral cervical region, and upper portion of the hind limb. Clonus was observed in the forelimbs. Clinicopathologic findings were normal, except for high serum globulin concentration, which was attributable mainly to an increase in the gamma-globulin fraction. Results of electroencephalography revealed almost continuous high-amplitude complexes in the occipital leads, interspersed with short runs of normal activity. There were generalized discharges, but these were not periodic. Current theory implicates the scrapie agent (prion) as the causal agent for BSE. The presence of scrapie in, and the possible entry of prion into bovine feedstuffs could result in the emergence of BSE in the United States.
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PMID:Bovine spongiform encephalopathy in a cow in the United Kingdom. 259 61

Lines of mice selectively-bred for High and Low-Activity in an open-field maze were tested for seizure susceptibility to three analeptics: flurothyl, pentylenetetrazol and bicuculline. The major finding was that two replicate High-Activity lines were more susceptible to myoclonic convulsions but less susceptible to clonic convulsions than their respective replicate Low-Activity lines. The major exception to this finding was that the High and Low-Activity lines did not differ for bicuculline-induced clonus although females tended to conform to the general pattern. These results are interesting because they demonstrate that diametrically opposite susceptibility to myoclonus and clonus is not an isolated phenomenon. Similar seizure susceptibility patterns and activity differences have also been reported for the Long-Sleep and Short-Sleep selectively-bred mouse lines. Further, since the progenitor population of the High-Activity and Low-Activity lines were developed from strains that were also part of the progenitor population of the Long-Sleep and Short-Sleep lines, it is hypothesized that some of the same alleles underwent selection in both selective-breeding programs.
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PMID:Differential convulsive susceptibility of high-activity and low-activity selected mice in response to GABA antagonists. 356 1


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