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tardive dyskinesia/sésamo
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7 resultados
The rat model of tardive dyskinesia: relationship between vacuous chewing movements and gross motor activity during acute and long-term haloperidol treatment.
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Tardive dyskinesia (TD) is a serious side-effect of neuroleptic treatment. In order to describe and analyse more thoroughly the rat model of TD, the behavior of the rats during cage testing was studied after acute and during long-term haloperidol (HAL) treatment. Rats were injected with HAL i.p. in
Central administration of the neurotensin receptor antagonist SR48692 attenuates vacuous chewing movements in a rodent model of tardive dyskinesia.
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Tardive dyskinesia is a movement disorder that develops in 20-30% of patients treated with chronic neuroleptics. Whilst the pathogenesis of tardive dyskinesia remains unclear, altered expression of neuropeptides in the basal ganglia has been implicated in its emergence. The peptide neurotensin is
Emergence of oral and locomotor activity in chronic haloperidol-treated rats following cortical N-methyl-D-aspartate stimulation.
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Neuroleptic-induced orofacial movements in rats have been widely utilized as an animal model of tardive dyskinesia (TD). The present study investigated the role of the oral motor cortex in these movements by applying direct cortical stimulation in rats exposed to chronic haloperidol. Rats received
Oral Dyskinesias and striatal lesions in rats after long-term co-treatment with haloperidol and 3-nitropropionic acid.
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The pathophysiologic basis of tardive dyskinesia remains unclear. It has been proposed that tardive dyskinesia may be a result of excitotoxic neurodegeneration in the striatum caused by a neuroleptic-induced increase in striatal glutamate release and impaired energy metabolism. To investigate this
Inhibition by memantine of the development of persistent oral dyskinesias induced by long-term haloperidol treatment of rats.
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1. Tardive dyskinesia (TD) is a serious side-effect of long-term treatment with neuroleptics. To investigate if neuroleptic-induced excessive stimulation of striatal glutamate receptors may underlie TD development, the effect of the NMDA antagonist, memantine (1-amino-3,5-dimethyladamantane), was
The effect of streptozotocin-induced diabetes on dopamine2, serotonin1A and serotonin2A receptors in the rat brain.
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The effect of streptozotocin (STZ)-induced diabetes and a combination of chronic treatment with haloperidol (HPD) on dopamine (DA)D2, serotonin (5-HT) 5-HT1A and 5-HT2A receptors was investigated in rat brain. Rats were randomly assigned to one of four groups: vehicle-vehicle, STZ-vehicle,
Effects of ceruletide on perioral movements and the dopamine receptor-adenylate cyclase system in rats chronically treated with fluphenazine.
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The effects of repeated administration of ceruletide (100 micrograms/kg/perday, i.p. for 3 days) on perioral movements and the striatal dopamine receptor adenylate cyclase system were examined in rats chronically treated with fluphenazine enanthate (FPZ) (25 mg/kg i.m. every 3 weeks for 30 weeks)
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