Fig. 3.

PRS effects on cortico-nigrostriatal synaptic transmission in adulthood (4-month-old rats).

Basal and depolarization-evoked release of glutamate or gamma-aminobutyric acid (GABA) in superfused striatal synaptosomes did not differ between PRS and unstressed control rats (glutamate n = 6 rats/group; GABA release n = 3 rats/group) (Fig. 3A). The striatal projection neurons of PRS rats did not show changes in resting membrane potential (n = 13 rats/group), spontaneous excitatory synaptic transmission (n = 10–15 rats/group), NMDA/AMPA ratio-mediated inward currents (n = 7 Ctrl, 9 PRS), or LTD of the excitatory synaptic transmission in response to high-frequency stimulation of the cortico-striatal pathway (n = 6 rats/group) (Fig. 3B). In the substantia nigra, PRS reduced the number of cells expressing the DA synthesizing enzyme tyrosine hydroxylase (TH) (n = 7–8 animals/group, Fig. 3C) but induced no difference in TH protein levels in the striatum (n = 6 adult rats/group, Fig. 3D). In contrast, in the striatum, PRS reduced high-affinity DA transporter (DAT) levels (n = 7 animals/group, Fig. 3D). In vivo micro-PET analysis of [¹⁸F]-DOPA uptake in the striatum (n = 4 animals/group) showed no difference between control and PRS rats (Fig. 3E). In contrast, PRS increased the steady-state levels of DA and its metabolites (DOPAC and HVA) in striatal homogenates (n = 10–12 rats/group, Fig. 3F). CONT vs. PRS *p < 0.05.