l-5-Hydroxytryptophan-induced myoclonus in guinea pigs: A model for the study of central serotonin-dopamine interactions

Volkman, Paul H.; Lorens, Stanley A.; Kindel, Gisela; Ginos, James Z.

doi:10.1016/0028-3908(78)90137-5

Cited by 34 publications

(5 citation statements)

References 29 publications

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“…Myoclonic jumping is a measure of restricted and repetitive behavior (Powell et al., 1999; Turner et al., 2001; Presti et al., 2004; Hines et al., 2008), and has been studied as a model of stereotypy extensively in guinea pigs (Volkman et al., 1978), and more recently in mice (Lalonde et al., 2002). The myoclonic jumping behavior was observed in 53 ± 9% of EL mice, and was absent in DDY mice (Fig.…”

Section: Resultsmentioning

confidence: 99%

The EL mouse: A natural model of autism and epilepsy

2011

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SUMMARYPurpose: Autism is a multifactorial disorder that involves impairments in social interactions and communication, as well as restricted and repetitive behaviors. About 30% of individuals with autism develop epilepsy by adulthood. The EL mouse has long been studied as a natural model of multifactorial idiopathic generalized epilepsy with complex partial seizures. Because epilepsy is a comorbid trait of autism, we evaluated the EL mouse for behaviors associated with autism. Methods: We compared the behavior of EL mice to agematched control DDY mice, a genetically related nonepileptic strain. The mice were compared in the open field and in the light-dark compartment tests to measure activity, exploratory behavior, and restricted and repetitive behaviors. The social transmission of food preference test was employed to evaluate social communication. Home-cage behavior was also evaluated in EL and DDY mice as a measure of repetitive activity.Key Findings: We found that EL mice displayed several behavioral abnormalities characteristic of autism. Impairments in social interaction and restricted patterns of interest were evident in EL mice. Activity, exploratory behavior, and restricted behavior were significantly greater in EL mice than in DDY mice. EL mice exhibited impairment in the social transmission of food preference assay. In addition, a stereotypic myoclonic jumping behavior was observed in EL mice, but was not seen in DDY mice. It is of interest to note that seizure activity within 24 h of testing exacerbated the autistic behavioral abnormalities found in EL mice. Significance: These findings suggest that the EL mouse expresses behavioral abnormalities similar to those seen in persons with autism. We propose that the EL mouse can be utilized as a natural model of autism and epilepsy.

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Section: Resultsmentioning

confidence: 99%

The EL mouse: A natural model of autism and epilepsy

2011

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“…A multitude of chemoconvulsant treatments are ameliorated by apomorphine (see Table V). Examples include the myoclonic jumping evoked by the administration of a high dose of 5-hydroxytryptophan to guinea pigs (Volkman et al, 1978;Weiner et al, 19791, and the secondarily generalised limbic motor seizures provoked in rats by a large systemic injection of the muscarinic cholinergic agonist pilocarpine (Turski et al, 1988). Focal seizures elicited by the chronic implantation of a cobalt-gelatine pellet (Dow et al, 1974;Farjo and McQueen, 1979) or by topical application of ouabain to the cortex (Stach and Kacz, 1977) are similarly suppressed by apomorphine.…”

Section: Effects Of Apomorphinementioning

confidence: 99%

“…Ergot derivatives such as lergotrile and piribedil are also good Dz agonists and potently anticonvulsant (An- lezark et al, 1981;Anlezark and Meldrum, 1975;Meldrum et al, 1975a;Riffee et al, 1981;Savoldi et al, 1979;Volkman et al, 1978;Weiner et al, 1979). By contrast, the prominent D2-stimulant action of the clinically useful antiparkinsonian drug pergolide only manifested as seizure protection in the pilocarpine (Al-Tajir and Starr, 1991a) and not the electroshock, PTZ, or strychnine models (Helton et al, 1992) and only protected spontaneously epileptic rats at toxic dose levels (Warter et al, 1988).…”

Section: Selective D Agonistsmentioning

confidence: 99%

The role of dopamine in epilepsy

Starr

1996

Synapse

241

157

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The clinical benefits of dopamine agonists in the management of epilepsy can be traced back over a century, whilst the introduction of neuroleptics into psychiatry practice 40 years ago witnessed the emergence of fits as a side effect of dopamine receptor blockade. Epidemiologists noticed a reciprocal relationship between the supposed dopaminergic overactivity syndrome of schizophrenia and epilepsy, which came to be regarded as a dopamine underactivity condition. Early pharmacological studies of epilepsy employed nonselective drugs, that often did not permit dopamine's antiepileptic action to be clearly dissociated from that of other monoamines. Likewise, the biochemical search for genetic abnormalities in brain dopamine function, as predeterminants of spontaneous epilepsy, proved largely inconclusive. The discovery of multiple dopamine receptor families (D1 and D2), mediating opposing influences on neuronal excitability, heralded a new era of dopamine‐epilepsy research. The traditional anticonvulsant action of dopamine was attributed to D2 receptor stimulation in the forebrain, while the advent of selective D1 agonists with proconvulsant properties revealed for the first time that dopamine could also lower the seizure threshold from the midbrain. Whilst there is no immediate prospect of developing D2 agonists or D1 antagonists as clinically useful antiepileptics, there is a growing awareness that seizures might be precipitated as a consequence of treating other neurological disorders with D2 antagonists (schizophrenia) or D1 agonists (parkinsonism). © 1996 Wiley‐Liss, Inc.

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“…In view of the data indicating serotonin induced and serotonin suppressed myoclonus in wakefulness, other neurotransmitters as etiological factors were investigated (Van Woert and Hwang, 1978;Growdon, 1979;Green and Grahame-Smith, 1974). Apomorphine and DA agonists were shown to suppress HTP-induced myoclonus and haloperidol or pimozide blocked this effect (Volkamn et al, 1978). L-Dopa induced myclonus was blocked by 5-HT antagonists and interrelations among receptors were proved (Klawans et al, 1975;Askenasy et al, 1980).…”

Section: Discussionmentioning

confidence: 98%

Is monoamine oxidase inhibitor induced myoclonus serotoninergically mediated?

Askenasy

Yahr

1988

J. Neural Transmission

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In the present study a single case observation of myoclonus during sleep-wave transition was monitored in a depressed patient treated with the monoamine oxidase inhibitor, phenelzine. The myoclonus had a rhythm of 1 c/second and lasted for two years, the duration of phenelzine treatment. Myoclonus appeared neither during wakefulness nor during sleep, but at wake-sleep-wake transitions. This "switch" myoclonus was associated with phasic muscle hyperactivity during REM sleep. Methysergide a 5-HT suppressor, decreased the switch myoclonus frequency and the REM muscle hyperactivity, indicating serotoninergic involvement in the mechanism of phenelzine induced myoclonus.

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l-5-Hydroxytryptophan-induced myoclonus in guinea pigs: A model for the study of central serotonin-dopamine interactions

Cited by 34 publications

References 29 publications

The EL mouse: A natural model of autism and epilepsy

The EL mouse: A natural model of autism and epilepsy

The role of dopamine in epilepsy

Is monoamine oxidase inhibitor induced myoclonus serotoninergically mediated?

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