Curcumin is a naturally occurring phenolic yellow chemical isolated from the rhizomes of the plant Curcuma longa (turmeric), and is a major component of the spice turmeric. Curcumin has protective effects against rotenone-induced neural damage in Parkinson's disease (PD). The present study aims at providing new evidence for the validity of the rotenone rat model of PD by examining whether neuronal activity in the hippocampus is altered. Male albino rats were treated with rotenone injections (2.5 mg/ml intraperitoneally) for 21 days. We examined the effects of curcumin (200 mg/kg) on behavior and electrophysiology in a rat model of PD induced by rotenone. Motor activity was assessed by cylinder test. The electrical activity of neurons was measured in hippocampus. Rotenone causes significant reduction of neuronal activity. The results show that curcumin can improve the motor impairments and electrophysiological parameters and may be beneficial in the treatment of PD.

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Rotenone is involved in the degeneration of dopaminergic neurons, and curcumin may prevent or effectively slow the progression of Parkinson disease (PD). Previous research has shown that the naturally occurring phenolic compound curcumin can reduce in ammation and oxidation, making it a potential therapeutic agent for neurodegenerative diseases. The present study involves investigation of rotenone induced histological changes in the brain areas, hippocampus using Nissl staining after 35 day of subcutaneous injection administration of rotenone in adult male rats. In this study, we investigated whether curcumin protects against rotenone-induced dopaminergic neurotoxicity in a rat model by in vivo electrical recording from Substantia nigra pars compacta (SNc). Curcumin treatment signi cantly improved electrical activity of neurons in the SNc of rotenone-induced PD model rats. The pattern of histological alterations corresponds with electrophysiological manifestations.

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Мы протестировали реакции нейронов ядра Дейтерса на двустороннюю высокочастотную стимуляцию паравентрикулярных и супраоптических ядер гипоталамуса (PVN & SON). Анализ спайковой активности проводился с помощью on-line выборки и специальной программы. Комплексные усредненные гистограммы времени и частоты перисобытий показывают усиление тормозных и возбуждающих тетенических (tetanic depression – TD, tetanic potentiation – TP, а также пост тетанических TP – PTP и пост тетанических TD – PTD) реакций нейронов ядра Дейтерса после инъекции богатого пролином пептида (PRP–1), достигая норме по окончании испытаний. Полученные результаты свидетельствуют о нейропротекторной эффективности PRP с участием ядер PVN и SON за счет модуляции тормозного контроля гипоталамуса. В гипоталамо-вестибулярном звене в качестве корректора патологических нарушений выступает гипоталамический пептидный нейромодулятор PRP. В условиях терапевтического действия PRP в процессах де- и регенерации нейронов LVN нельзя исключить участие реального ГАМК-ергического торможения в механизмах возникновения TD и PTD. / We tested the responses of Deiters nucleus neurons to bilateral high-frequency stimulation of the paraventricular and supraoptic nuclei of the hypothalamus (PVN & SON). The analysis of spike activity was carried out using on-line sampling and a special program. Complex averaged histograms of the time and frequency of peri-events show an increase in inhibitory and excitatory tethenic (tetanic depression – TD, tetanic potentiation – TP, as well as post-tetanic TP – PTP and post-tetanic TD – PTD) reactions of Deiters nucleus neurons after injection of a proline-rich peptide (PRP–1), reaching the norm at the end of the test. The results obtained indicate the neuroprotective efficacy of PRP involving the PVN and SON nuclei by modulating the inhibitory control of the hypothalamus. In the hypothalamic-vestibular link, the hypothalamic peptide neuromodulator PRP acts as a corrector of pathological disorders. Under the conditions of the therapeutic effect of PRP in the processes of de- and regeneration of LVN neurons, the involvement of real GABAergic inhibition in the mechanisms of TD and PTD cannot be ruled out.