Knockdown of PSD-95/SAP90 delays the development of neuropathic pain in rats. Academic Article

abstract

• Our previous work has shown that PSD-95/SAP90 is required for NMDA receptor-mediated thermal hyperalgesia. To address the role of PSD-95/SAP90 in chronic pain, the present study investigated the effect of the deficiency of PSD-95/SAP90 on nerve injury-induced neuropathic pain. Following unilateral L5 spinal nerve injury, mechanical and thermal hyperalgesia developed within 3 days and persisted for 9 days or longer on the injured side. The intrathecal administration of antisense oligodeoxynucleotide specifically against PSD-95/SAP90, but not sense or missense oligodeoxynucleotide, dose-dependently delayed the onset of tactile allodynia and thermal hyperalgesia. These results suggest that PSD-95/SAP90 might be involved in the central mechanisms of the development of chronic neuropathic pain.

authors

• Tao, Feng

published proceedings

• Neuroreport

altmetric score

• 3

author list (cited authors)

• Tao, F., Tao, Y. X., Gonzalez, J. A., Fang, M., Mao, P., & Johns, R. A.

citation count

• 69

complete list of authors

• Tao, F||Tao, YX||Gonzalez, JA||Fang, M||Mao, P||Johns, RA

publication date

• January 2001

publisher

• Wolters Kluwer  Publisher

published in

• NeuroReport  Journal

keywords

• Animals
• Behavior, Animal
• Disease Models, Animal
• Disks Large Homolog 4 Protein
• Dose-Response Relationship, Drug
• Foot
• Hyperalgesia
• Intracellular Signaling Peptides And Proteins
• Male
• Membrane Proteins
• Nerve Tissue Proteins
• Neuralgia
• Oligodeoxyribonucleotides, Antisense
• Pain Measurement
• Pain Threshold
• Peripheral Nerve Injuries
• Peripheral Nerves
• Peripheral Nervous System Diseases
• Physical Stimulation
• Rats
• Rats, Sprague-Dawley
• Spinal Nerve Roots

Digital Object Identifier (DOI)

• 10.1097/00001756-200110290-00022

start page

• 3251

end page

• 3255

volume

• 12

issue

• 15

URL

• http://dx.doi.org/10.1097/00001756-200110290-00022