Activity, Motor Control & Coordination
Pain - Thermal Allodynia / Hyperalgesia
Pain - Spontaneous Pain - Postural Deficit
Pain - Mechanical Allodynia / Hyperalgesia
Anxiety & Depression Disorder
Learning/Memory - Attention - Addiction
Physiology & Respiratory Research
Metabolism - Food & Drink Intake
Pain
Metabolism
Motor control
Neurodegeneration
Cross-disciplinary subjects
Muscular system
General activity
Mood Disorders
Other disorders
Joints
Central Nervous System (CNS)
Sensory system
Authors
R. Lalonde, M. Dumont, E. Paly, J. London, C. Strazielle.
Lab
Faculté de Médecine et de Pharmacie, Université de Rouen, INSERM U614, Rouen, France ; CHUM/St-Luc, Montréal, Canada ; Université de Paris 7 Denis-Diderot, EA 3508 Paris, France ; Laboratoire de Pathologie Moléculaire et Cellulaire des Nutriments, Faculté
Journal
Brain Research Bulletin
Abstract
SOD1 is one of several overexpressed genes in Down's syndrome. In order to dissect genetic causes of the syndrome, hemizygous human wild-type SOD1 transgenic mice were compared to FVB/N non-transgenic controls at 3 months of age in the SHIRPA primary screen of neurologic function as well as in tests of motor activity and coordination. The responsiveness of SOD1/wt transgenic mice to visual and somatosensory stimuli was reduced in placing, pinna, corneal, and toe-pinch tests. In addition, SOD1/wt transgenic mice crossed fewer segments on a stationary beam. On the contrary, there was no intergroup difference for motor activity and anxiety in open-field and emergence tests and for latencies before falling on the stationary beam, coat-hanger, and rotorod. These results indicate mild deficits in sensorimotor responsiveness in a mouse model expressing human SOD1 and that the overexpressed gene may be responsible for some Down symptoms.
BIOSEB Instruments Used:
Aron Test or Four Plates Test (LE830),Rotarod (BX-ROD)
