Alterations in synaptic input to motoneurons during partial spinal cord injury.

An acute animal model (dorsal hemisection of the spinal cord in the decerebrate cat preparation) has been developed that closely mimics the spasticity in humans that occurs subsequent to partial spinal cord injury and hemiparetic stroke. In this animal model, there are severe disruptions in the pattern of recruitment and rate modulation of motoneurons. The cellular mechanisms of these deficits are being studied with a combined experimental/computer simulation approach. The initial studies indicate that changes in the intrinsic properties of motoneurons are not important, which means the mechanism for changes in recruitment and rate patterns must reside in an alteration in the organization of the synaptic input to motoneurons. Computer simulation studies of the effects of different synaptic inputs on motoneuron outputs show that inhibitory inputs can, under certain conditions, generate substantial disruptions in recruitment and rate modulation. Recent data indicate that the monoamines noradrenalin and serotonin, which are released by fiber tracts originating in the brainstem, may play an important role in maintaining normal levels of inhibition in spinal circuits. Pharmacological interventions based on the monoamines may provide effective means of reducing the deficits in recruitment and rate modulation.