Hericium erinaceus Rescued Motor and Purkinje Cell Deficits in Rat Model of 3-Acetylpyridine-Induced Cerebellar Ataxia

Abstract

Introduction: Cerebellar ataxia is a neurodegenerative disorder that is characterized by irreversible cerebellar atrophy and motor coordination deficits. There is no effective treatment to treat this debilitating disorder. Recently, Hericium erinaceus (H.E.), a culinary-medicinal mushroom has been shown to enhance neuroplasticity and antioxidative functions in both in vitro and in vivo findings. In this study, we tested the hypothesis of neuroprotective effects of H.E. in rescuing motor deficits in a rat model of acquired cerebellar ataxia. Materials and Methods: Rat model of cerebellar ataxia was generated by single intraperitoneal injection of 3-acetylpyridine (3-AP; 40 mg/kg). Animals received daily injections of either H.E. (10 mg/kg or 25 mg/kg) or saline for 3 weeks; and they were tested for motor coordination and balance. Brain samples were processed for gene expression study of neuroplasticity-related function, and morphological study of the cerebellum by haematoxylin-eosin staining. Results and Discussion: Our results demonstrated that 25 mg/kg H.E. significantly improved motor coordination and balance in ataxic rats. Gene expression analysis revealed significant normalization of Dcx, Nestin, TrkB, and CREB levels in 25 mg/kg H.E. treated rats, compared to the saline group. Purkinje cell deformation was found in all 3-AP-treated groups except for animals that received 25 mg/kg H.E. Regular morphology of Purkinje cells was retained in the cerebellar cortex of 25 mg/kg H.E treated and non-3-AP control animals. Conclusion: H.E. administration potentially rescued the motor and cerebellar Purkinje cell deficits in ataxic rats, indicating neuroprotective effects against 3-APinduced cerebellar ataxia.