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 chro
nic pain, the present study investigated the effect of the deficiency of PS
D-95/SAP90 on nerve injury-induced neuropathic pain. Following unilateral L
5 spinal nerve injury, mechanical and thermal hyperalgesia developed within
3 days and persisted for 9 days or longer on the injured side. The intrath
ecal administration of antisense oligodeoxynucleotide specifically against
PSD-95/SAP90, but not sense or missense oligodeoxynucleotide, dose-dependen
tly delayed the onset of tactile allodynia and thermal hyperalgesia. These
results suggest that PSD-95/SAP90 might be involved in the central mechanis
ms of the development of chronic neuropathic pain. NeuroReport 12:3251-3255
(C) 2001 Lippincott Williams & Wilkins.