Recurrent facilitation of spinal reflexes

Antidromic volleys in muscle nerves may facilitate monosynaptic reflexes originating from neighboring motoneurons. This facilitation has been studied in spinal cats. It is at its peak with a conditioning-test interval of 20 to 30 msec., and can last 50 to 100 msec. The threshold of facilitation is about the same as that of recurrent inhibition. Both phenomena appear to be activated by stimulation of the large motor axons. The latency of facilitation seems to be longer than that of recurrent inhibition by approximately 1 msec., suggesting the presence of at least one more synaptic delay. Facilitation often follows an inhibition of variable depth and duration. Frequently, however, the facilitation is not preceded by inhibition, and therefore it cannot be a rebound effect. The pharmacological properties of facilitation resemble those of recurrent inhibition. Dihydro-beta-erythroidine¹ partially blocks facilitation; the peak is decreased and occurs earlier, and the duration is shortened. Eserine increases the duration of facilitation and inhibition and sometimes enhances their magnitude. It is concluded that recurrent facilitation is mediated by the cholinergic axon collaterals, and that at least two interneurons are located between collateral and motoneuron. Possible mechanisms of facilitation are discussed.     

Manipulations of spinal cord excitability evoke developmentally-dependent compensatory changes in the lamprey spinal cord

We have examined homeostatic or compensatory plasticity evoked by tonic changes in spinal cord excitability in the lamprey, a model system for investigating spinal cord function. In larval animals, reducing excitability by incubating in tetrodotoxin or the glutamate receptor antagonists CNQX or CNQX/AP5 for 20–48 h resulted in a diverse set of cellular and synaptic changes that together were consistent with an increase in spinal cord excitability. Similar changes occurred to a tonic increase in excitation evoked by incubating in high potassium physiological solution (i.e. responses were unidirectional). We also examined developmental influences on these effects. In animals developing from the larval to adult form effects were reduced or absent, suggesting that at this stage the spinal cord was more tolerant of changes in activity levels. Responses had returned in adult animals, but they were now bi-directional (i.e. opposite effects were evoked by an increase or decrease in excitability). The spinal cord can thus monitor and adapt cellular and synaptic properties to tonic changes in excitability levels. This should be considered in analyses of spinal cord plasticity and injury.     

Development of spinal cord bioelectric activity in spinal chick embryos and its behavioral implications

Embryonic behavior of the chick is the product of spontaneous multiunit burst discharges within the ventral spinal cord. The present study describes the ontogeny of spinal cord burst discharges in embryos which were deprived of brain input by removing several neural tube segments of 2-day embryos at cervical or mid-thoracic levels. Characteristics of bioelectric activity present in both intact and chronically transected cords are: (a) the appearance of spike discharges; (b) the organization of unit discharges into synchronized multiunit bursts; (c) the establishment of intracord synchronization of burst discharges over wide expanses of cord tissue; (d) an increase in burst duration and complexity at 7 days due to the appearance of the burst afterdischarge; (e) an increase in the amount of burst activity from 6 to 13 days followed by a decline until hatching at 21 days; (f) a shift from periodic to irregular patterns of burst activity at 13 days; and (g) the existence of the cord burst discharge as a correlate of embryonic movement. Several differences were found between burst activity from chronic spinal and intact embryos: (a) cervical spinal embryos were significantly less active than controls from 15 through 19 days; and (b) long sequences of unusual repetitive burst afterdischarges appeared in chronic spinal embryos by 13 days. The results indicate that the transected embryonic spinal cord is remarkably autogenous in function, although patterns of activity unique to the transected cord appear and increase in prominence during later stages of incubation.     

Lumbar spinal stenosis.

Lumbar spinal stenosis, the results of congenital and degenerative constriction of the neural canal and foramina leading to lumbosacral nerve root or cauda equina compression, is a common cause of disability in middle-aged and elderly patients. Advanced neuroradiologic imaging techniques have improved our ability to localize the site of nerve root entrapment in patients presenting with neurogenic claudication or painful radiculopathy. Although conservative medical management may be successful initially, surgical decompression by wide laminectomy or an intralaminar approach should be done in patients with serious or progressive pain or neurologic dysfunction. Because the early diagnosis and treatment of lumbar spinal stenosis may prevent intractable pain and the permanent neurologic sequelae of chronic nerve root entrapment, all physicians should be aware of the different neurologic presentations and the treatment options for patients with spinal stenosis.