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

F. Tao; Y. X. Tao; J. A. Gonzalez; M. Fang; P. Mao; R. A. Johns

doi:10.1097/00001756-200110290-00022

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

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

School of Medicine

Research output: Contribution to journal › Article › peer-review

64 Scopus citations

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.

Original language	English (US)
Pages (from-to)	3251-3255
Number of pages	5
Journal	Neuroreport
Volume	12
Issue number	15
DOIs	https://doi.org/10.1097/00001756-200110290-00022
State	Published - Oct 29 2001

Keywords

Antisense technology
Hyperalgesia
Intrathecal injection
Neuropathic pain
PSD-95/SAP90
Spinal central sensitization
Spinal cord

ASJC Scopus subject areas

General Neuroscience

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10.1097/00001756-200110290-00022

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title = "Knockdown of PSD-95/SAP90 delays the development of neuropathic pain in rats",

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.",

keywords = "Antisense technology, Hyperalgesia, Intrathecal injection, Neuropathic pain, PSD-95/SAP90, Spinal central sensitization, Spinal cord",

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AU - Tao, F.

AU - Tao, Y. X.

AU - Gonzalez, J. A.

AU - Fang, M.

AU - Mao, P.

AU - Johns, R. A.

PY - 2001/10/29

Y1 - 2001/10/29

N2 - 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.

AB - 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.

KW - Antisense technology

KW - Hyperalgesia

KW - Intrathecal injection

KW - Neuropathic pain

KW - PSD-95/SAP90

KW - Spinal central sensitization

KW - Spinal cord

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

Abstract

Keywords

ASJC Scopus subject areas

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