| Abstrakt: |
In neurodegenerative diseases, mainly in Parkinson's disease (PD), neurodegeneration involves antinociceptive centers, which is accompanied by persistent pain not relieved by opioids. In this study, in three experimental series carried out on 13 white mongrel rats, we analyzed the impulse activity of 390 single neurons of the raphe magnus nucleus (RMG) elicited by high-frequency stimulation (HFS) of the periaqueductal gray matter (PAG) under normal conditions, in the rotenone model of PD, and under conditions of hydrocortisone protection. Based on the programmatic mathematical analyses of the degree of manifestation of the average frequency of post-stimulus depressor and excitatory synaptic effects, a sharp increase in the tetanic and post-tetanic excitatory effects was revealed in the PD model. At the same time, there was a multiple decrease in the number of neurons responding with depressor synaptic reactions, and with an increase in those, responding with excitatory reactions. This effect was due to excessive excitability, attesting to a well-known compensatory increase in the excitability of the preserved RMG neurons, accompanied by their inevitable degenerative damage. After hydrocortisone exposure, the depressor synaptic reactions increased drastically with a significant increase in the number of the neurons involved, indicating a neutralization of the excitatory reactions that resulted in their natural decay. Considering the protective role of depressor reactions that we found previously, the analogous effect of hydrocortisone is quite evident. Moreover, on the PD model, RMG neurons during HFS of the PAG exhibited a pronounced (3- and 5-fold) increase in the pre-stimulus frequency of activity that preceded the depressor post-stimulus synaptic reactions. Hydrocortisone protection led to a significant (7- and 9-fold) reduction in the frequency of pre-stimulus impulse activity that preceded excitatory post-stimulus manifestations of activity, clearly arguing in favor of the protective effect of hydrocortisone. In the PD model, the post-stimulus frequency of RMG neuronal activity, accompanied by excitatory synaptic effects, far (7–5-fold and more) exceeded the norm, also attesting to a huge increase in the excitability of neurons. Under hydrocortisone protection, there was a sharp (18.3- and 17.7-fold) reduction in the post-stimulus frequency of impulse activity in RMG neurons in the PD model, accompanied by the excitatory post-stimulus effects. The data obtained herein demonstrate a pronounced protective effect of hydrocortisone due to increased inhibitory synaptic effects. [ABSTRACT FROM AUTHOR] |
