Back to Search Start Over

Motor behavioral abnormalities and histopathological findings in middle aged male Wistar rats inoculated with cerebrospinal fluid from patients with Amyotrophic Lateral Sclerosis

Authors :
Auderlan M. Gois
José M.M. Bispo
Lívia C.R.F. Lins
Katty A.A.L. Medeiros
Marina F. Souza
Edson R. Santos
Jileno F. Santos
Alessandra M. Ribeiro
Regina H. Silva
Marcelo O.R. Paixão
José F.S. Leopoldino
Murilo Marchioro
José R. Santos
Deise M.F. Mendonça
Source :
Current Research in Behavioral Sciences, Vol 3, Iss , Pp 100069- (2022)
Publication Year :
2022
Publisher :
Elsevier, 2022.

Abstract

Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease associated with loss of upper and lower motor neurons in the primary motor cortex and spinal cord, respectively. Motor deficits are the main clinical features observed in patients with the disease. However, it has been suggested that the presence of neurotoxic factors in the cerebrospinal fluid (CSF) from ALS patients causes loss of motor neurons. The present study investigated the motor and histopathological changes induced by intracerebroventricular (ICV) infusion of CSF from ALS patients in middle aged male Wistar rats. Middle aged male rats were divided into three groups: (1) control group, animals injected with artificial CSF solution; (2) N-ALS group, animals injected with CSF from volunteers without neurological disease; and (3) ALS group, animals inoculated with CFS from a patient with definite ALS. After surgical and infusion procedures, animals were evaluated in different motor tests (grip strength; catalepsy and open field tests). Moreover, animals’ spinal cords were histologically investigated. We observed that ALS-CSF infusion reduced grip strength and led to motor changes and reduction in the number of motor neurons and glial cells in thoracic and lumbar regions of spinal cord. However, CSF N-ALS caused reduction of nerve and glial cells in the thoracic but not in the lumbar region. Our data suggest that ALS-CSF is associated with neurodegenerative mechanisms observed in ALS pathology.

Details

Language :
English
ISSN :
26665182
Volume :
3
Issue :
100069-
Database :
Directory of Open Access Journals
Journal :
Current Research in Behavioral Sciences
Publication Type :
Academic Journal
Accession number :
edsdoj.84867656057b42ce882e4d0917048357
Document Type :
article
Full Text :
https://doi.org/10.1016/j.crbeha.2022.100069