Characterization of a cerebral palsy-like model in rats: Analysis of gait pattern and of brain and spinal cord motor areas

• Published in: International journal of developmental neuroscience Vol. 60; no. 1; pp. 48 - 55
• Main Authors: dos Santos, Adriana Souza, de Almeida, Wellington, Popik, Bruno, Sbardelotto, Bruno Marques, Torrejais, Márcia Miranda, de Souza, Marcelo Alves, Centenaro, Lígia Aline
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 01-08-2017; Elsevier BV
• Subjects: Animal model; Animals; Asphyxia; Bacteria; Balance; Brain; Caudate-putamen; Central pattern generator; Cerebral palsy; Cerebral Palsy - chemically induced; Cerebral Palsy - complications; Cerebral Palsy - physiopathology; Coordination; Corpus callosum; Disease Models, Animal; Female; Gait; Gait Disorders, Neurologic - chemically induced; Gait Disorders, Neurologic - etiology; Gait Disorders, Neurologic - physiopathology; Genetic crosses; Glial cells; Humans; Limbs; Lipopolysaccharide; Lipopolysaccharides; Motor Activity - drug effects; Motor Cortex - drug effects; Motor Cortex - pathology; Motor Cortex - physiopathology; Motor neurons; Motor Neurons - drug effects; Motor Neurons - pathology; Motor task performance; Neostriatum; Offspring; Paralysis; Perinatal asphyxia; Perinatal exposure; Pregnancy; Rats; Rats, Wistar; Rodents; Sensorimotor restriction; Sensorimotor system; Somatosensory cortex; Species Specificity; Spinal cord; Spinal Cord - drug effects; Spinal Cord - pathology; Spinal Cord - physiopathology; Ventral horn; Ventricle; Ventricles (cerebral); P0; Animal model; Cerebral palsy; Perinatal asphyxia; P2; BBB; PVL; i.p; G17; P30; CP; LPS; P45; P49; TNF-α; P48; P29; CTG; P28; Lipopolysaccharide; Sensorimotor restriction; CPG; IL1-β
• ISSN: 0736-5748; 1873-474X
• DOI: 10.1016/j.ijdevneu.2017.04.005

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•Pre-natal infection, asphyxia and sensorimotor restriction alter gait pattern in rats.•Motor impairments were attenuated over time.•Sensorimotor cortex and dorsal striatum exhibited an increased number of glial cells.•White matter injury were not observed in this cerebral palsy animal model.•The interventions used did not affect soma area of motoneurons in the spinal cord.
In an attempt to propose an animal model that reproduces in rats the phenotype of cerebral palsy, this study evaluated the effects of maternal exposure to bacterial endotoxin associated with perinatal asphyxia and sensorimotor restriction on gait pattern, brain and spinal cord morphology. Two experimental groups were used: Control Group (CTG) − offspring of rats injected with saline during pregnancy and Cerebral Palsy Group (CPG) − offspring of rats injected with lipopolysaccharide during pregnancy, submitted to perinatal asphyxia and sensorimotor restriction for 30days. At 29days of age, the CPG exhibited coordination between limbs, weight-supported dorsal steps or weight-supported plantar steps with paw rotation. At 45days of age, CPG exhibited plantar stepping with the paw rotated in the balance phase. An increase in the number of glial cells in the primary somatosensory cortex and dorsal striatum were observed in the CPG, but the corpus callosum thickness and cross-sectional area of lateral ventricle were similar between studied groups. No changes were found in the number of motoneurons, glial cells and soma area of the motoneurons in the ventral horn of spinal cord. The combination of insults in the pre, peri and postnatal periods produced changes in hindlimbs gait pattern of animals similar to those observed in diplegic patients, but motor impairments were attenuated over time. Besides, the greater number of glial cells observed seems to be related to the formation of a glial scar in important sensorimotor brain areas.