L.V Darbinyan1*, L.E Hambardzumyan1, L.P Manukyan1, K.V Simonyan2, S.H Badalyan1, N.V Sargsyan1 and V.H Sarkisian1
Parkinson's disease (PD) is a progressive neurodegenerative disorder that affects nerve cells, or neurons, in the part of the brain that controls movement. A hallmark feature of PD is the degeneration of the dopamine neurons in the substantia nigra (SN) pars compacta and the consequent striatal dopamine deficiency. Yet, the pathogenesis of PD remains unclear.The lack of dopamine causes the primary symptoms of Parkinson's disease - tremor, slowness of movement, muscle stiffness and balance problems. In vivo animal models have simulated most, although not all, of the hallmarks of PD and are useful for testing new neuroprotective approaches. Research is devoted to the study of systemic compensatory reactions of the rat's brain developing in response to rotenone-induced animal model of PD under the conditions of neuroprotective intervention of Curcumin. This has raising expectations for the development of new neuroprotective therapies for the prevention of PD. Male albino rats were treated with rotenone injections (2.5 mg/ml intraperitoneally) for 21 days. We examined the effects of neuroprotector curcumin (200 mg/kg) on behavior and the electrical activity of hippocampus neurons measured in response to high frequency stimulation (HFS) of entorhinal cortex (EC). In the hippocampus, the excitatory and inhibitory synapses between EC and CA3 pyramidal cells expresses robust forms of short-term plasticity, such as frequency facilitation (post-tetanic potentiation-PTP) and depression (post-tetanic depression- PTD). Motor activity was assessed by cylinder test. The results showed that Rotenone causes significant reduction of neuronal activity, whereas curcumin can improve the motor impairments and electrophysiological parameters and may be beneficial in the treatment of PD. Curcumin significantly prevented rotenone-induced impairment of hippocampal synaptic plasticity, which is likely mediated via dysfunction of mitochondrial complex I. It alleviated the deficits behavior in rats as the rearing frequencies of animals were enhanced.