Effects of combined hemotoxic and anterolateral spinal lesions on nociceptive sensitivity.
The effects of spinal lesions on reactions of rats to nociceptive electrocutaneous stimulation (ES) were evaluated by measuring the speed of operant escape responses, the magnitude of hindlimb flexion reflexes and the amplitude of reflex vocalizations. ES intensities ranging from 0.1 to 0.8mA were delivered to either hindpaw of rats that were trained to terminate stimulation (perform an escape response) with one forelimb. Unilateral thoracic lesions within the lateral column were produced by surgically transecting axons, with or without insertion of blood-soaked Gelfoam into the lesion cavity. The latter procedure was intended to standardize and maximize hemotoxic damage to the gray matter at the lesion site. The speed of conscious escape responses to all intensities was reduced contralaterally and to comparable extents following each type of lesion. Involvement of mid-lateral axons was an important determinant of contralateral deficits in escape responding. Escape speed for ipsilateral stimulation was not affected by the lesion without intentional insertion of blood but was reliably increased by addition of blood to the lesion site. Flexion reflexes were substantially decreased contralaterally and slightly decreased ipsilaterally, in accordance with previous investigations of anterolateral lesion effects in monkeys. Early (reflex) vocalizations were essentially eliminated for stimulation contralateral to the lesions, but vocalizations following ipsilateral stimulation were little affected. Postoperative variations in behavioral responsivity over time were not accounted for by pre- and post-estrous stages of the estrous cycle. The principal finding of this study is that hemotoxic accompaniments of a spinal lesion produce hyperalgesia for nociceptive stimulation applied ipsilaterally to segments well caudal to the lesion. This finding indicates that hemotoxic injury of the gray matter near an anterolateral spinal lesion enhances the excitation of certain rostral structures that receive nociceptive information.
Vierck
Charles J
CJ
Department of Neuroscience, University of Florida College of Medicine, Gainesville, FL, USA Department of Physiology, School of Medicine, University of North Carolina, Chapel Hill, NC 27599, USA.
Light
Alan R
AR
D000818:Animals; D003216:Conditioning, Operant / Q000502:physiology*; D002818:Cordotomy / Q000009:adverse effects*; D004558:Electric Stimulation; D004924:Escape Reaction / Q000502:physiology*; D005260:Female; D006470:Hemorrhage / Q000503:physiopathology*; D006614:Hindlimb / Q000502:physiology; D006930:Hyperalgesia / Q000503:physiopathology; D010147:Pain Measurement; D051381:Rats; D020318:Rats, Long-Evans; D012018:Reflex / Q000502:physiology; D013118:Spinal Cord Diseases / Q000503:physiopathology*; D014828:Vocalization, Animal / Q000502:physiology