НЕЙРОПРОТЕКТОРНЫЙ ЭФФЕКТ ФОРСКОЛИНА И ЕГО ВЛИЯНИЕ НА МИТОХОНДРИАЛЬНУЮ ДИСФУНКЦИЮ В НЕЙРОНАХ ПЕРВИЧНОЙ КУЛЬТУРЫ МОЗЖЕЧКА КРЫС

It is commonly accepted that an increase in cyclic adenosine monophposphate (cAMP) production triggers neuroprotection related signaling cascades. It was interesting to evaluate the influence of forskolin induced cAMP production by adenylate cyclase on the neurotoxic action of glutamate in rat cerebellar neurons. We also aimed to determine the participants of the involved signaling cascade. In our experiments we used proteinkinase A (PKA) inhibitor, proteinkinase C (PKC) inhibitor - chelerythrine, and calmodulin-dependent kinase II (CaMKII) inhibitor - KN93 to determine that forskolin (1 p.m) mediated neuroprotection during long-term 24 h treatment with glutamate (100 p.m) involves PKA and СаМЫ1. Further analysis of mitochondrial dysfunction during glutamate treatment revealed that forskolin can prevent the drop mitochondrial membrane potential in cerebellar neurons, which is usually observed in excytotoxic stress.