Fig. 1

Increased anxiety and depression-like behavior in the rotenone model of Parkinson’s disease. Rotenone-treated rats (red bars) were unable to run on the rotating rod in the rotarod test (A) and they moved less in the open field test (OFT) (B). The increased anxiety level was proven by longer time spent in the periphery of the OFT arena (C). Rotenone-treated rats drank less sweetened water in the sucrose preference test (SPT) suggesting increased anhedonia (D). Relative adrenal (E) and thymus (F) weights as well as bodyweight (G) data suggest increased hypothalamus–pituitary–adrenal axis activity in the rotenone-treated group compared to vehicle (oil) injected rats (black bars). Tyrosine-hydroxylase (TH, green in H, I)—alpha-synuclein (αSYN, red in H, I) double labeling in the substantia nigra pars compacta (SNpc) revealed reduced SNpc/TH-immunoreactive (ir) cell count (J) in rotenone-treated rats. Cytoplasmic alpha-synuclein-ir inclusions (see arrowhead in insert of panel I) were observed upon rotenone treatment in SNpc/TH neurons (K). The assessment of microglia morphology in the SNpc by TH (green in L, M)—ionized calcium binding adaptor molecule 1 (IBA1, red in L, M) double labeling revealed increased activity score upon rotenone treatment (N). TH (green in P, Q)—glial fibrillary acidic protein (GFAP, red in P, Q) double labeling revealed also increased astrogliosis (O) in rotenone-treated rats. TH (red in R, S)—NeuN (green, R, S) labeling in the caudate-putamen (CPu) revealed reduced dopaminergic fiber density in rotenone-treated rats (T) occasionally with focal pattern (see the border of focal fiber loss area indicated by arrowheads in panel S). Rotenone treatment did not induce neuron loss in the striatum (U). *p < 0.05, **p < 0.01, ***p < 0.001 in Student’s t test or in Mann–Whitney U test in N and O. n = 8–12. Bars: 50 µm