The spatial organization of central sensitization of hind limb flexor reflexes in the decerebrated, spinalized rabbit.
This study was designed to investigate the relationship between the location of a noxious stimulus and the magnitude and duration of the plastic effects induced by that stimulus in withdrawal reflexes acting about the knee and the ankle, in rabbits. Reflexes were evoked in the nerves to the anterior tibial and semitendinosus flexor muscles by electrical stimulation at the toes. Repetitive, high intensity electrical stimulation of nerve trunks (sural, medial gastrocnemius, superficial peroneal, tibial, 100 pulses, 20 V, 1 ms at 0.5 Hz) was generally found to be a poor method for inducing central sensitization in these flexor reflexes. 'Natural' noxious stimulation induced more reliable enhancement of both reflexes. Mechanical (clamp) or chemical (mustard oil) stimulation of the heel induced prolonged (median duration >30 min) increases in reflexes to both muscles. Mechanical (clamp and superficial pinch) or chemical (mustard oil) stimulation of the toes, and injection of bradykinin into the gastrocnemius muscles or into the soft tissues of the sole of the foot, also led to enhancement of both reflexes, with the median duration of potentiation between 7 and 30 min. The effects obtained from deep tissue stimulation were generally weaker than those obtained after stimulation of superficial structures. These data show that there were no major differences in the effects obtained from the heel vs the toes, or between the two reflexes. It appears that the spatial organization of the spinal mechanisms underlying central sensitization of flexor withdrawal reflexes is rather more crudely drawn than that pertaining to the reflexes themselves. Furthermore, the data indicate that in the present preparation, afferents from deep tissues are no more effective in generating central sensitization than those from superficial structures.
Clarke
R W
RW
Division of Animal Physiology, School of Bioscience, University of Nottingham, Sutton Bonington Campus, Loughborough, LE12 5RD, UK. robert.clarke@nottingham.ac.uk
Harris
J
J
D000344:Afferent Pathways / Q000166:cytology / Q000502:physiology; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology; D003655:Decerebrate State / Q000503:physiopathology*; D004558:Electric Stimulation; D005260:Female; D006614:Hindlimb / Q000294:innervation; D008297:Male; D018482:Muscle, Skeletal / Q000294:innervation*; D009270:Naloxone / Q000494:pharmacology; D009292:Narcotic Antagonists / Q000494:pharmacology; D009619:Nociceptors / Q000502:physiology*; D011817:Rabbits; D012026:Reflex, Stretch / Q000187:drug effects / Q000502:physiology*; D013979:Tibial Nerve / Q000166:cytology / Q000502:physiology
D009292:Narcotic Antagonists; D009270:Naloxone; D001920:Bradykinin