Does abnormal spinal reciprocal inhibition lead to co-contraction of antagonist motor units? A modeling study.
It is suggested that co-contraction of antagonist motor units perhaps due to abnormal disynaptic I(a) reciprocal inhibition is responsible for Parkinsonian rigidity. A neural model of Parkinson's disease bradykinesia is extended to incorporate the effects of spindle feedback on key cortical cells and examine the effects of dopamine depletion on spinal activities. Simulation results show that although reciprocal inhibition is reduced in DA depleted case, it doesn't lead to co-contraction of antagonist motor neurons. Implications to Parkinsonian rigidity are discussed.
Cutsuridis
Vassilis
V
Department of Computing Science and Mathematics, University of Stirling, Stirling FK9 4LA, Scotland. vcu@cs.stir.ac.uk
D000200:Action Potentials; D003198:Computer Simulation; D006801:Humans; D008433:Mathematics; D008959:Models, Neurological; D009046:Motor Neurons / Q000502:physiology*; D009433:Neural Inhibition / Q000502:physiology*; D010300:Parkinson Disease / Q000473:pathology*; D013116:Spinal Cord / Q000473:pathology* / Q000503:physiopathology*