THE EFFECTS OF HYDROCORTISONE ON SYNAPTIC PROCESSES IN PARKINSON'S DISEASE UNDERLYING THE POTENTIAL THERAPEUTIC STRATEGIES.

The study was carried out electrophysiological effects of hydrocortisone for protection on the prelimbic cortex (PrL) neurons in rats, particularly in response to high-frequency stimulation (HFS) of the Caudate-Putamen nuclear complex (CPu) on the models of Parkinson's disease (PD). The study involved 19 rats of the Albino line, each weighing 250 gr. The rats were divided into three experimental groups: intact, rotenone model of Parkinson's disease (PD), and rats with PD but treated with hydrocortisone for protection. Extracellular recording was conducted to measure the impulse activity of single neurons in the prelimbic cortex (PrL) particularly in response to high-frequency stimulation (HFS) of the Caudate-Putamen nuclear complex (CPu) on the models of PD and PD treated with hydrocortisone for protection. In rats with the PD model, there was a decrease in post-stimulus synaptic depressor tetanic effects compared to the norm. This means that the ability of synapses to depress their activity after stimulation was reduced in PD. Conversely, excitatory effects increased in PD rats compared to the norm. This indicates an increase in the excitatory response of neurons in the PD model. When hydrocortisone was applied in PD rats, the frequency of impulse activity dropped sharply, even falling below the levels observed in the normal condition. This indicates that hydrocortisone treatment mitigated the heightened neural activity induced by PD, possibly returning it to a more normal state. Overall, these findings suggest that PD alters synaptic responses and neural activity in the PrL, and hydrocortisone treatment seems to reverse some of these effects.