Title : Effects of prenatal androgen exposure on Purkinje cell morphology in the cerebellum of female rats
Abstract:
Background: Polycystic ovarian syndrome (PCOS) is a complex endocrine disorder typically characterized by hyperandrogenism, ovulatory dysfunction, and polycystic ovaries. Prenatal exposure to elevated androgen levels, particularly testosterone, has been linked to changes in brain structure and function, including excessive growth of dendritic spines and traits associated with autism spectrum disorder (ASD). This is particularly relevant as research shows a link between polycystic ovarian syndrome (PCOS) and ASD. Prenatally androgenized (PNA) female rats serve as a model for studying the effects of prenatal androgen exposure on the brain. The cerebellum, integral to motor coordination and control, has emerged as a point of interest due to its sensitivity to hormonal fluctuations. Research suggests that these fluctuations may disrupt the expression of calbindin, a neuroprotective calcium-binding protein, and affect the soma size in Purkinje cells, the cerebellar cells responsible for fine-tuning and coordinating voluntary movements.
Objective: The primary objective of this study was to examine the soma size and expression of calbindin in Purkinje cells in the cerebellum of PNA female rats as compared to control rats. Methods: Cerebellar tissue samples were collected from both PNA rats and control rats at 16 weeks of age. Cerebella were sectioned, and Purkinje cells were traced at 40x magnification; comparisons of the soma areas were conducted. Additional cerebellum slices were incubated with antibodies to determine calbindin expression.
Results: The Purkinje soma area sizes were significantly greater in cerebellar lobes 2, 5, 6a, and 9b in PNA rats. However, the soma size was significantly smaller in lobe 9a of the PNA rat. There was no significant difference in calbindin expression.
Conclusions: The data indicate that increased prenatal exposure to testosterone significantly affects the morphology, particularly the soma size, of Purkinje cells in the cerebellum. This disruption potentially contributes to the motor deficits observed in the PNA rat model.
