Corticosteroid Regulation of Excitatory and Inhibitory Synaptic Activity in the Basomedial Amygdala under Entorhinal Cortex Activation in Parkinson’s Disease

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Abstract Background: Parkinson’s disease (PD) is a neurodegenerative disorder that extends beyond its motor manifestations to include emotional and cognitive disturbances. The amygdala, particularly the basomedial nucleus (BMA), plays a crucial role in emotional regulation and receives dopaminergic input from the substantia nigra and ventral tegmental area. Dysfunction of this pathway may contribute to affective deficits in PD. Methods: We investigated the excitatory and inhibitory post-stimulus manifestations of BMA neuronal activity during high-frequency stimulation (HFS) of the entorhinal cortex (ENT) in a rotenone-induced PD model and under hydrocortisone administration. Extracellular recordings were performed in three groups of rats: controls, PD-model animals, and hydrocortisone-treated PD rats. Spike responses were analyzed for tetanic depression (TD), tetanic potentiation (TP), post-tetanic depression (PTD), and post-tetanic potentiation (PTP). Results: PD-model animals exhibited marked alterations in BMA neuronal excitability, characterized by enhanced TD and TP sequences, reflecting an excitatory–inhibitory imbalance. Hydrocortisone administration partially restored normal firing dynamics, reducing depressive responses and normalizing excitatory activity toward control levels. Conclusion: These findings indicate that hydrocortisone exerts a stabilizing effect on BMA neuronal responsiveness during ENT stimulation in the PD model. The results suggest that glucocorticoids may protect limbic neuronal circuits from PD-related dysfunction, offering potential therapeutic implications for the management of affective and emotional disturbances in Parkinson’s disease.

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