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Influence of Aminooxyacetic Acid, a -Aminobutyrate Transaminase Inhibitor, on Hereditary Spastic Defect in the Mouse.
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1962
Year
Psychotropic MedicationGeneticsPharmacotherapyExperimental PharmacologyAminooxyacetic AcidHereditary Spastic DefectRepeated InjectionsSocial SciencesMolecular PharmacologyPharmacological StudyMotor ActivityNeurologyHereditary Neurological DisorderMolecular NeuroscienceBehavioural PharmacologyInherited Metabolic DiseaseBehavioral PharmacologyNeuropharmacologyPharmacology-Aminobutyrate Transaminase InhibitorMovement DisordersClinical DisordersNeurophysiologyPhysiologyDegenerative DiseaseClinical PharmacologyNeuroscienceMedicine
Experiments were performed on mice with a hereditary neurological disorder characterized by spasm. Simple tests which were used to assess response to drugs included measurement of righting time after being placed on the back, and evaluation of degree of tremor and extent of flexibility and alertness. When single doses of Dilantin, trimethadione, or aminooxyacetic acid were administered intraperitoneally to the spastic mice, only the latter substance was found to be effective in decreasing the symptoms. Subcutaneously injected aminooxyacetic acid in doses of 5 to 15 μg/g produced marked improvement which was sustained for 12-24 hours or more. In some animals which received repeated injections of the drug there was a depression of motor activity, decreased alertness, and loss in weight. Two-dimensional paper chromatograms of extracts of brains of the spastic mice showed no significant alteration of distribution of ninhydrin-reactive constituents by comparison with normal controls.