ADMINISTRAÇÃO HIPOCAMPAL DE EXPOLISSACARÍDEO EM MODELO DE NEUROTOXICIDADE INDUZIDA POR INIBIÇÃO DA GLUTAMATO DESCARBOXILASE

Abstract

Neurotoxicity may manifest as an acute, subacute and chronic presenting several symptoms including seizures. In the event of neurotoxicity induced cellular mechanisms may occur as apoptosis, oxidative stress, mitochondrial dysfunction and inhibition of neurogenesis. The glutamate decarboxylase is an enzyme which acts directly on the metabolism of neurotransmitters GABA (γ-aminobutyric acid). The action of GABA is modulated allosterically by a variety of chemical substances that interact with distinct binding sites of the GABA. The β-glucans have been considered as the natural products that may be useful in the prevention and treatment of various diseases in humans. Thus the aim of this research was to evaluate the effect of acute injection of lasiodisplodana From exopolysaccharide on the neurochemical and behavioral consequences of inhibition of glutamate decarboxylase. The study used 24 Wistar rats (Rattus norvegicus), 60 days, subjected to controlled environmental conditions. The animals were weighed and divided into 4 groups, with groups: 1 salt, 2 penicillamine, 3 exopolysaccharide (EPS) + penicillamine and 4 exopolysaccharide (EPS). The results obtained in the experiment and presented with M ± SD, behavioral animals showed some behavioral changes, but not coming to convulse, was not observed any histopathological changes in the brain tissue. In the results observed that lipid peroxidation penicillamine compared to saline gave an increase (Penicillamine = 2.36 nMol / mg, saline = 0.31 nMol / mg) when done pretreatment with exopolysaccharides (EPS), and injected after penicillamine observed a decrease (Penicillamine = 2.36 nMol / mg; Penicillamine + EPS = 0.79 nMol / mg) and are presented as mean standard deviation. In conclusion penicillamine cause neurotoxicity, with the expolissacarídeo played an important role in mitigating the effects caused by penicillamine.