S-100
Chronic Administration of Propranolol Promotes Attenuation of Motor Damage and Dopaminergic Protection in a Model of Parkinsonism Induced by Reserpine
Maria Micaelle Gomes Tavares1,2,5, Maria Camila Santos de Oliveira1,2,5, Mylaine Santos Mendonça1,2,5, Tamiris Rodrigues Santos1,2,5, José Carlos Junior da Silva Lima1,2,5, Iasmin de Carvalho Dantas1,2,3, Caroline Izidro Andrade1,2,3, Heitor Franco Santos1,2,5, Katty Anne Amador de Lucena Medeiros1,2,4, Lívia Cristina Rodrigues Ferreira Lins1,2,5, José Ronaldo dos Santos1,2,3, Alessandra Mussi Ribeiro6, Regina Helena da Silva6, Auderlan Mendonça de Gois1,2,3
  1. Federal University of Sergipe
  2. Behavioral and Evolutionary Neurobiology Laboratory
  3. Department of Biosciences
  4. Nursing Department
  5. Department of Physiology
  6. Federal University of São Paulo Baixada Santista – UNIFESP
Presenting Author:
Maria Micaelle Gomes Tavares
micaelletavares1999@gmail.com
Parkinson's disease (PD) is a motor disorder characterized by dopaminergic and noradrenergic dysfunction, culminating in motor symptoms in non-motor ones. Chronic use of beta-blockers has been associated with an increased risk of PD, but this association may be a causal effect. We evaluated the effect of chronic propranolol administration on motor, non-motor, and immunoreactive changes in a reserpine-induced parkinsonism model. Wistar rats were subjected to chronic administration of propranolol, 10, 20, or 40 mg/kg, subcutaneously (s.c.) daily, for 60 days (CEUA: 6294030423). After 30 days of experimentation, the animals were induced to parkinsonism with reserpine 0.1 mg/kg, s.c. injection every 48h, subjected to behavioral tests and immunohistochemistry for tyrosine hydroxylase (TH). Propranolol, dose-dependently, attenuated the motor impairment in catalepsy and increased the rearing time at a dose of 10 mg/kg. Furthermore, doses of 10 and 40 mg/kg promoted a decrease in oral tremor time and the number of vacuous chewing, and only the 10 mg/kg dose improved the animals' working memory. Conversely, propranolol 20 and 40 mg/kg increased TH immunoreactivity in the SNpc, and only the 40 mg/kg dose in the VTA. Thus, propranolol may alleviate motor deficits and protect against dopaminergic depletion induced by reserpine. Studies are needed to understand the pathophysiological and neuroprotective mechanisms of propranolol associated with PD.