Intraperitoneal administration of afobazole in a dose of 0.1 mg/kg over 2 weeks after repeated modeling of intracerebral post-traumatic hematoma reduces animal mortality, decreases motor coordination disturbances, and improves learning and memory processes in rats.
Aim. To examine the cerebrovascular, neuroprotective and antiarrhythmic properties of fabomotizole (brand name Afobazole).
Materials and methods. A comprehensive study of fabomotizole's effects on the blood supply, morphology and neuropsychology of the rat brain in various experimental disorders. We recorded cerebral blood flow and studied brain morphology in models of local permanent and global transient ischaemia, haemorrhagic brain damage, combined cerebrovascular and cardiovascular pathology, cardiac arrhythmias, and assessed the neuropsychological status. We measured the levels of GABA, glutamic acid, nerve growth factor, and heat shock protein (HSP70).
Results. Fabomotizole improves blood supply, limits the area of injury, normalizes pathological brain changes in localized cerebral ischaemia, and eliminates neuropsychological damage in models of ischaemic and haemorrhagic stroke. The drug increases cerebral blood flow in ischaemic and haemorrhagic stroke, myocardial infarction and, to a greater extent, in combined cerebrovascular and coronary disease. Fabomotizole acts through the cerebrovascular GABAAergic system, as well as having significant antiarrhythmic properties.
Conclusions. Fabomotizole should be considered not only as an anxiolytic, but also as a drug with potential clinical efficacy in cerebrovascular disease, with concomitant coronary disease and cardiac arrhythmias.
Rats with the Parkinsonian syndrome induced by systemic injection of the neurotoxin 1-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) develop extrapyramidal disorders (oligokinesia, tremor, and rigidity) which depend on the dose and duration of action of MPTP. At 15 and 30 mg/kg MPTP impairs the learning of the conditioned passive avoidance response, shortens both stages of sleep, particularly the paradoxical (REM) stage, and prolongs the period of wakefulness. The mnestic function disturbance is not associated with extrapyramidal disorders, since it develops in their absence. In MPTP-treated rats memory and sleep disorders are interrelated.
Key Words: extrapyramidal disorders; Parkinsonian syndrome; sleep patternIn addition to extrapyramidal symptoms (tremor, oligokinesia, and rigidity) and characteristic autonomic disturbances, patients with parkinsonism have impaired intellectual and mnestic functions and develop sleep disorders [5][6][7][8]. The causes of these abnormalities and their relation to pathogenesis and therapy of Parkinson's disease so far remain unclear. The Parkinsonian syndrome has Laboratory of Psychopharmacology, Institute of Pharmacology, Russian Academy of Medical Sciences, Moscow been modeled with the use of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin which damages dopaminergic neurons of the striatum thus inducing extrapyramidal disturbances [2,9]. Chronic administration of MPTP in low doses to monkeys impairs the learning of Conditioned responses, the effect being reversed by dopaminergic agonists [10].In this study we examined mnestic functions and sleep disorders in rats with the Parkinsonian syndrome induced by MPTP.
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