Microelectrophysiological Studies of the Ratio of Excitatory to Inhibitory Synaptic Processes in the Corticonigral Projection in a Model of Parkinson’s

Experiments on 23 white male rats (250 g) analyzed the spike activity of individual neurons in the substantia nigra pars compacta (SNc, 242 neurons, n = 11) and substantia nigra pars reticulata (SNr, 289 neurons, n = 12) during high-frequency stimulation of the primary motor cortex (M1)in normal animals and in animals with a rotenone model of Parkinson’s disease (BP). SNc neurons in the model of PD showed a complete absence of depressor effects induced by stimulation, though tetanic potentiation was accompanied by posttetanic potentiation and depression at levels 1.65 and 2.02 times greater than in normal animals. In SNr neurons in normal animals, tetanic potentiation, accompanied by post-tetanic potentiation and depression, was 2.37 times greater than tetanic depression, while in the model of PD the levels of both depressor and excitatory activity induced by stimulation were below normal. Spike activity frequency in SNc and SNr neurons preceding and accompanying stimulation was significantly greater than normal in the model of PD. This is evidence for excitotoxicity accompanying neurodegenerative damage, which is completed by neuron apoptosis and death. In SNr neurons, both depressor and excitatory reactions accompanying stimulation were markedly dominant over those in SNc neurons, which is evidence for more extensive cortical projections to the SNr. Furthermore, SNc neurons demonstrated greater susceptibility to pathological changes due to poststimulus depressor effects than SNr neurons, with formation of more marked excitatory effects, which is evidence of a greater involvement of the SNc in PD. In the model of PD, lacking stimulation-induced depressor effects and more marked excitatory effects in SNc neurons, SNr neurons retained their depressor reactions and relatively decreased excitatory reactions, which is evidence of a lower level of susceptibility of SNr neurons to excitotoxicity, extreme increases in the excitability of surviving neurons compensating for the lack of excitation of dead cells.