The nonsynaptic plasticity in Parkinson's disease: Insights from an animal model

Authors

  • Mônica P.C. Viegas Laboratory of Experimental and Computational Neuroscience, Department of Biosystems Engineering, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, MG, Brazil https://orcid.org/0009-0002-5179-7104
  • Luiz E.C. Santos Laboratory of Experimental and Computational Neuroscience, Department of Biosystems Engineering, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, MG, Brazil https://orcid.org/0000-0002-5465-2333
  • Mayra C. Aarão Laboratory of Experimental and Computational Neuroscience, Department of Biosystems Engineering, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, MG, Brazil https://orcid.org/0009-0002-9127-667X
  • Samyra G. Cecilio Laboratory of Experimental and Computational Neuroscience, Department of Biosystems Engineering, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, MG, Brazil https://orcid.org/0000-0003-1474-410X
  • Carla A. Scorza Neuroscience Discipline, Escola Paulista de Medicina da Universidade Federal de São Paulo (EPM/UNIFESP), São Paulo, SP, Brazil SCImago image Centro de Neurociências e Saúde da Mulher “Professor Geraldo Rodrigues de Lima”, Escola Paulista de Medicina da Universidade Federal de São Paulo (EPM/UNIFESP), São Paulo, SP, Brazil https://orcid.org/0000-0001-7810-4748
  • Marcelo A. Moret SENAI ‒ Departamento Regional da Bahia, Centro Integrado de Manufatura e Tecnologia, Bahia, BA, Brazil https://orcid.org/0000-0003-0051-6309
  • Josef Finsterer Neurology & Neurophysiology Center Vienna, Vienna, Austria https://orcid.org/0000-0002-2304-4175
  • Fulvio A. Scorza Neuroscience Discipline, Escola Paulista de Medicina da Universidade Federal de São Paulo (EPM/UNIFESP), São Paulo, SP, Brazil SCImago image Centro de Neurociências e Saúde da Mulher “Professor Geraldo Rodrigues de Lima”, Escola Paulista de Medicina da Universidade Federal de São Paulo (EPM/UNIFESP), São Paulo, SP, Brazil https://orcid.org/0000-0002-0694-8674
  • Antônio-Carlos G. Almeida Laboratory of Experimental and Computational Neuroscience, Department of Biosystems Engineering, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, MG, Brazil https://orcid.org/0000-0003-4893-338X
  • Joana M. Medrado Laboratory of Experimental and Computational Neuroscience, Department of Biosystems Engineering, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, MG, Brazil https://orcid.org/0009-0008-9382-9315
  • Arthur C. Pires Laboratory of Experimental and Computational Neuroscience, Department of Biosystems Engineering, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, MG, Brazil https://orcid.org/0000-0001-5718-5200
  • Antônio M. Rodrigues Laboratory of Experimental and Computational Neuroscience, Department of Biosystems Engineering, Universidade Federal de São João del-Rei (UFSJ), São João del-Rei, MG, Brazil https://orcid.org/0000-0002-2678-9180

DOI:

https://doi.org/10.1016/

Keywords:

Parkinson's disease, Animal model, Non-synaptic mechanisms

Abstract

Background:The 6-OHDA nigro-striatal lesion model has already been related to disorders in the excitability and synchronicity of neural networks and variation in the expression of transmembrane proteins that control intra and extracellular ionic concentrations, such as cation-chloride cotransporters (NKCC1 and KCC2) and Na+/K+-ATPase and, also, to the glial proliferation after injury. All these non-synaptic mechanisms have already been related to neuronal injury and hyper-synchronism processes.Objective:The main objective of this study is to verify whether mechanisms not directly related to synaptic neurotransmission could be involved in the modulation of nigrostriatal pathways. Methods: Male Wistar rats, 3 months old, were submitted to a unilateral injection of 24 µg of 6-OHDA, in the striatum (n= 8). The animals in the Control group (n= 8) were submitted to the same protocol, with the replacement of 6-OHDA by 0.9% saline. The analysis by optical densitometry was performed to quantify the immunoreactivity intensity of GFAP, NKCC1, KCC2, Na+/K+-ATPase, TH and Cx36. Results: The 6-OHDA induced lesions in the striatum, were not followed by changes in the expression cation-chloride cotransporters and Na+/K+-ATPase, but with astrocytic reactivity in the lesioned and adjacent regions of the nigrostriatal. Moreover, the dopaminergic degeneration caused by 6-OHDA is followed by changes in the expression of connexin-36. Conclusions: The use of the GJ blockers directly along the nigrostriatal pathways to control PD motor symptoms is conjectured. Electrophysiology of the striatum and the substantia nigra, to verify changes in neuronal synchronism, comparing brain slices of control animals and experimental models of PD, is needed.

Downloads

Download data is not yet available.

Downloads

Published

2023-09-13

Issue

Vol. 78 (2023)

Section

Original Articles

How to Cite

Viegas, M. P., Santos, L. E. ., Aarão, M. C. ., Cecilio, S. G. ., Scorza, C. A. ., Moret, M. A. ., Finsterer, J. ., Scorza , F. A. ., Almeida, A.-C. G. ., Medrado, J. M. ., Pires, A. C. ., & Rodrigues, A. M. . (2023). The nonsynaptic plasticity in Parkinson’s disease: Insights from an animal model. Clinics, 78, 100242 . https://doi.org/10.1016/