Akademik Veri Yönetim Sistemi
Biotechnic and Histochemistry, 2026 (SCI-Expanded, Scopus)
Parkinson’s disease (PD) is a progressive neurodegenerative disorder associated with aging. It is characterized by both motor and non-motor symptoms, including cognitive impairment, mood disturbances, sleep disruption, sexual dysfunction, and weight loss. These symptoms may precede a clinical diagnosis. Sex-related differences in PD, influenced by estrogen’s neuroprotective effects and testosterone deficiency, contribute to a higher prevalence and severity of the disease in males. Male rats received daily subcutaneous injections of rotenone (2 mg/kg) for 20 days to establish a PD model, which enabled the investigation of central dopaminergic degeneration and peripheral testicular effects. Tyrosine hydroxylase (TH) immunoreactivity in the substantia nigra pars compacta (SNpc) was assessed alongside the testicular expression of GPR30, GPR120, and GPR125 in the testes using immunohistochemical and immunofluorescence techniques. Rotenone-treated animals exhibited significant weight loss (z = −4.292, p < 0.001), reduced TH expression in the SNpc, and hallmark PD pathology including Lewy body-like inclusions, Lewy neurites, and halo-like structures around dopaminergic neuron nuclei. Testicular analysis revealed a time-dependent decline in GPR protein expression. GPR30 was found in spermatids and interstitial cells, GPR120 was found predominantly in Leydig cells, and GPR125 was found in interstitial tissue, Sertoli cells, and spermatocytes. These findings suggest that the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) may affect testicular function via testosterone-dependent regulation of GPR30, GPR120, and GPR125 expression. This highlights the systemic nature of PD and its potential impact on male reproductive health. Alterations in testicular G Protein-Coupled Receptors (GPCRs) may serve as peripheral biomarkers of disease progression, emphasizing the importance of considering endocrine and reproductive dysfunction in both experimental models and the clinical management of PD.