Segmental neuropathic pain does not develop in male rats with complete spinal transections.
In a previous study using male rats, a correlation was found between the development of "at-level" allodynia in T6-7 dermatomes following severe T8 spinal contusion injury and the sparing of some myelinated axons within the core of the lesion epicenter. To further test our hypothesis that this sparing is important for the expression of allodynia and the supraspinal plasticity that ensues, an injury that severs all axons (i.e., a complete spinal cord transection) was made in 15 male rats. Behavioral assessments were done at level throughout the 30-day recovery period followed by terminal electrophysiological recordings (urethane anesthesia) from single medullary reticular formation (MRF) neurons receiving convergent nociceptive inputs from receptive fields above, at, and below the lesion level. None of the rats developed signs of at-level allodynia (versus 18 of 26 male rats following severe contusion). However, the terminal recording (206 MRF neurons) data resembled those obtained previously post-contusion. That is, there was evidence of neuronal hyper-excitability (relative to previous data from intact controls) to high- and low-threshold mechanical stimulation for "at-level" (dorsal trunk) and "above-level" (eyelids and face) cutaneous territories. These results, when combined with prior data on intact controls and severe/moderate contusions, indicate that (1) an anatomically incomplete injury (some lesion epicenter axonal sparing) following severe contusion is likely important for the development of allodynia and (2) the neuronal hyper-excitability at the level of the medulla is likely involved in nociceptive processes that are not directly related to the conscious expression of pain-like avoidance behaviors that are being used as evidence of allodynia.
Hubscher
Charles H
CH
Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, Kentucky 40292, USA.
Kaddumi
Ezidin G
EG
Johnson
Richard D
RD
D000200:Action Potentials / Q000502:physiology; D000344:Afferent Pathways / Q000293:injuries / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D001369:Axons / Q000473:pathology; D004195:Disease Models, Animal; D006930:Hyperalgesia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D008526:Medulla Oblongata / Q000503:physiopathology; D009415:Nerve Net / Q000503:physiopathology; D009437:Neuralgia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology; D009619:Nociceptors / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012154:Reticular Formation / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000150:complications* / Q000473:pathology / Q000503:physiopathology*; D014855:Wallerian Degeneration / Q000150:complications / Q000473:pathology / Q000503:physiopathology