Alteration in rate modulation of reflexes to lumbar motoneurons after midthoracic spinal cord injury in the rat. I. Contusion injury.
This study investigated the regulation of reflex excitability in normal and midthoracic contusion-injured animals. Recent observations revealed that rate depression, a rate-modulatory process that decreases reflex excitability, was significantly decreased following experimental midthoracic contusion injury. The present experiments were performed to extend those studies and to determine if posttetanic potentiation (PTP), a rate-modulatory process that increases reflex excitability, also was altered in lumbar monosynaptic reflexes (MSRs) following midthoracic contusion injury. In normal animals, a mean PTP of 160% of the pretetanus control was observed at 30 sec following tetanus of the tibial MSR. The decay of the PTP in normal animals followed a rapid initial, then a more gradual pattern, before returning to pretetanus values by 5 min posttetanus. Following midthoracic contusion injury, the maximal (unpotentiated) MSRs were significantly increased in amplitude, whereas the percent potentiation of the PTP of the tibial MSRs was significantly decreased. PTP decay in postcontusion animals was significantly more gradual than observed in normal animals and followed a single decay process. Further analysis of rate depression of tibial MSRs in normal animals revealed that the attenuation pattern produced by stimulation within the lower range of test frequencies was different from that produced by stimulation at the higher test frequencies. Following contusion, rate depression of tibial MSRs was significantly reduced at all test frequencies. These physiological changes in the stretch reflex neural pathway are discussed relative to the development of spasticity.
Department of Neuroscience, University of Florida Health Science Center, Gainesville 32610-0244, USA.
F J
FJ
Thompson
R
R
Parmer
P J
PJ
Reier
D000818:Animals; D003288:Contusions / Q000150:complications / Q000503:physiopathology*; D004195:Disease Models, Animal; D004558:Electric Stimulation; D019054:Evoked Potentials, Motor; D005260:Female; D017774:Long-Term Potentiation / Q000502:physiology; D009046:Motor Neurons / Q000502:physiology; D009128:Muscle Spasticity / Q000209:etiology* / Q000503:physiopathology; D009434:Neural Pathways / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time / Q000502:physiology; D012021:Reflex, Abnormal / Q000502:physiology*; D012023:Reflex, Monosynaptic / Q000502:physiology*; D012026:Reflex, Stretch / Q000502:physiology*; D012044:Regression Analysis; D013119:Spinal Cord Injuries / Q000150:complications / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000502:physiology; D013746:Tetany / Q000503:physiopathology; D013979:Tibial Nerve / Q000502:physiology; D013997:Time Factors