Molecular, anatomical, physiological, and behavioral studies of rats treated with buprenorphine after spinal cord injury.
Acute pain is a common symptom experienced after spinal cord injury (SCI). The presence of this pain calls for treatment with analgesics, such as buprenorphine. However, there are concerns that the drug may exert other effects besides alleviation of pain. Among those reported are in vitro changes in gene expression, apoptosis, and necrosis. In this investigation, the effect of buprenorphine was assessed at the molecular, behavioral, electrophysiological, and histological levels after SCI. Rats were injured at the T10 thoracic level using the NYU impactor device. Half of the animals received buprenorphine (0.05 mg/kg) for 3 consecutive days immediately after SCI, and the other half were untreated. Microarray analysis (n = 5) was performed and analyzed using the Array Assist software. The genes under study were grouped in four categories according to function: regeneration, apoptosis, second messengers, and nociceptive related genes. Microarray analysis demonstrated no significant difference in gene expression between rats treated with buprenorphine and the control group at 2 and 4 days post-injury (DPI). Experiments performed to determine the effect of buprenorphine at the electrophysiological (tcMMEP), behavioral (BBB, grid walking and beam crossing), and histological (luxol staining) levels revealed no significant difference at 7 and 14 DPI in the return of nerve conduction, functional recovery, or white matter sparing between control and experimental groups (p > 0.05, n = 6). These results show that buprenorphine (0.05 mg/kg) can be used as part of the postoperative care to reduce pain after SCI without affecting behavioral, physiological, or anatomical parameters.
Santiago
José M
JM
Department of Physiology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico.
Rosas
Odrick
O
Torrado
Aranza I
AI
González
María M
MM
Kalyan-Masih
Priya O
PO
Miranda
Jorge D
JD
D000701:Analgesics, Opioid / Q000009:adverse effects / Q000494:pharmacology*; D000818:Animals; D017209:Apoptosis / Q000187:drug effects / Q000235:genetics; D002047:Buprenorphine / Q000009:adverse effects / Q000494:pharmacology*; D004195:Disease Models, Animal; D019054:Evoked Potentials, Motor / Q000187:drug effects / Q000502:physiology; D005260:Female; D020233:Gait Disorders, Neurologic / Q000139:chemically induced / Q000503:physiopathology; D005786:Gene Expression Regulation / Q000187:drug effects* / Q000502:physiology; D008124:Locomotion / Q000187:drug effects / Q000502:physiology; D009416:Nerve Regeneration / Q000187:drug effects / Q000235:genetics; D009419:Nerve Tissue Proteins / Q000235:genetics; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology; D009619:Nociceptors / Q000187:drug effects / Q000378:metabolism; D020411:Oligonucleotide Array Sequence Analysis; D010148:Intractable Pain / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function / Q000187:drug effects* / Q000502:physiology; D015290:Second Messenger Systems / Q000187:drug effects / Q000235:genetics; D013119:Spinal Cord Injuries / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D016896:Treatment Outcome
D000701:Analgesics, Opioid; D009419:Nerve Tissue Proteins; D002047:Buprenorphine