02345nas a2200229   4500008004100000022001400041245005800055210005700113260001200170300001400182490000600196520170800202653002201910100002001932700002201952700002001974700001801994700002002012700002102032700001502053856004702068       1996                        eng d  a1063-652800aTherapeutic neural effects of electrical stimulation.0 aTherapeutic neural effects of electrical stimulation  c12/1996  a218–2300 v43 aThe use of a functional neuromuscular stimulation (FNS) device can have therapeutic effects that persist when the device is not in use. Clinicians have reported changes in both voluntary and electrically assisted neuromuscular function and improvements in the condition of soft tissue. Motor recovery has been observed in people with incomplete spinal cord injury, stroke, or traumatic brain injury after the use of motor prostheses. Improvement in voluntary dorsiflexion and overall gait pattern has been reported both in the short term (several hours) and permanently. Electrical stimulation of skin over flexor muscles in the upper limb produced substantial reductions for up to 1 h in the severity of spasticity in brain-injured subjects, as measured by the change in torque generation during ramp-and-hold muscle stretch. There was typically an aggravation of the severity of spasticity when surface stimulation reached intensities sufficient to also excite muscle. Animals were trained to alter the size of the H-reflex to obtain a reward. The plasticity that underlies this operantly conditioned H-reflex change includes changes in the spinal cord itself. Comparable changes appear to occur with acquisition of certain motor skills. Current studies are exploring such changes in humans and animals with spinal cord injuries with the goal of using conditioning methods to assess function after injury and to promote and guide recovery of function. A better understanding of the mechanisms of neural plasticity, achieved through human and animal studies, may help us to design and implement FNS systems that have the potential to produce beneficial changes in the subject's central nervous systems.10aTreatment Outcome1 aDaly, Janis, J.1 aMarsolais, E., B.1 aMendell, L., M.1 aRymer, W., Z.1 aStefanovska, A.1 aWolpaw, Jonathan1 aKantor, C.  uhttp://www.ncbi.nlm.nih.gov/pubmed/897394802723nas a2200241   4500008004100000022001400041245010800055210006900163260001200232300001400244490000700258520200700265653002702272653000802299653001102307653001502318653002502333653001602358100002302374700001902397700001802416856004702434       1991                        eng d  a0014-481900aAlterations in motoneuron properties induced by acute dorsal spinal hemisection in the decerebrate cat.0 aAlterations in motoneuron properties induced by acute dorsal spi  c02/1991  a539–5480 v833 aUsing intracellular recording techniques, we studied the response characteristics of two separate populations of triceps surae motoneurons in unanesthetized decerebrate cats, recorded before and after low thoracic hemisection of the spinal cord. In each preparation, we studied the response properties of one group of motoneurons and the protocol was then repeated for a separate group, immediately following the dorsal hemisection. In each group, we examined both the minimum firing rates of motoneurons during intracellular current injection and a range of cellular properties, including input resistance, rheobase current and afterhyperpolarization time course and magnitude. Although earlier studies from this laboratory have shown substantial reductions in minimum firing rate in reflexively active motoneurons in the hemisected decerebrated preparation, the response of motoneurons to intracellular current injection in the current preparation proved to be quite different. Minimum firing rates were either normal or even somewhat higher in the post-lesion group, while the time course of the afterhyperpolarization was shortened. Moreover, these effects were not evenly distributed across the motoneuron pool. The rate effect was most evident in motoneurons with higher conduction velocity, while the afterhyperpolarization effect occurred predominantly in motoneurons with lower conduction velocity. Neither of these effects could be accounted for by lesion-induced changes in other cellular properties. We conclude that tonically active neurons with descending axons traversing dorsolateral white matter may influence both the discharge characteristics and membrane properties of spinal motoneurons in novel ways, presumably by modifying voltage or calcium activated motoneuronal conductances. The previously described reactions in the firing rate of motoneurons after such lesions appear to be mediated by different means, perhaps by alterations in synaptic input from segmental interneurons.10aafterhyperpolarization10acat10alesion10amotoneuron10arepetitive discharge10aSpinal Cord1 aCarp, Jonathan, S.1 aPowers, R., K.1 aRymer, W., Z.  uhttp://www.ncbi.nlm.nih.gov/pubmed/202619601802nas a2200217   4500008004100000022001400041245009300055210006900148260001200217300001400229490000700243520113900250653003101389653001401420653001601434653001901450653002701469100002301496700001801519856004701537       1986                        eng d  a0014-481900aEnhancement by serotonin of tonic vibration and stretch reflexes in the decerebrate cat.0 aEnhancement by serotonin of tonic vibration and stretch reflexes  c03/1986  a111–1220 v623 aThe effects of pharmacological manipulation of serotonergic systems on spinal reflexes were determined in the unanesthetized decerebrate cat. The prolonged motor output that continues after cessation of high frequency longitudinal tendon vibration was strongly enhanced by the serotonin reuptake blocker fluoxetine and the serotonin precursor 5-hydroxytryptophan, and was decreased by the serotonin receptor antagonist methysergide. In addition, both dynamic and static stretch reflex stiffness was markedly increased by fluoxetine and 5-hydroxytryptophan, while methysergide produced a decrease in stretch reflex stiffness. These powerful effects on tonic vibration and stretch reflexes could not be explained by drug-induced alterations in muscle spindle primary afferent discharge. In light of other recent results on serotonin-mediated effects on motoneurons, we believe that the effects of these agents result from modification of an intrinsically mediated prolonged depolarization of spinal neurons. However, the possibility that these drugs modify longlasting discharge in associated interneuronal pathways cannot be ruled out.10abistable neuronal behavior10aserotonin10aSpinal Cord10astretch reflex10atonic vibration reflex1 aCarp, Jonathan, S.1 aRymer, W., Z.  uhttp://www.ncbi.nlm.nih.gov/pubmed/3007191