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Peripheral glutamate receptors contribute to mechanical hyperalgesia in a neuropathic pain model of the rat.
Neuroscience. 2004; 128(1):169-76.N

Abstract

We hypothesized that glutamate (Glu) released from the peripheral terminals of primary afferents contributes to the generation of mechanical hyperalgesia following peripheral nerve injury. Nerve injury was performed on rats with a lumbar 5 spinal nerve lesion (L5 SNL), which was preceded by L5 dorsal rhizotomy (L5 DR) to avoid the potential central effects induced by L5 SNL through the L5 dorsal root. Mechanical hyperalgesia, as evidenced by a reduction in paw withdrawal threshold (PWT), was short-lasting (<6 days) after L5 DR, but persistent (>42 days) after L5 SNL preceded by L5 DR. When an intraplantar injection into the affected hind paw was given immediately before L5 SNL, non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (20 nmol), group-I metabotropic Glu (mGlu) receptor antagonist DL-amino-3-phosphonopropionic acid (DL-AP3; 70 nmol), and selective group-II mGlu receptor agonist 4-aminopyrrolidine-2,4-dicarboxylate (APDC; 20 nmol) delayed the onset of PWT reduction for 1-4 days. However, this onset was not affected by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainate receptor antagonist 2,3-dioxo-6-nitro-1,2,3,4,-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX; 100 nmol). When the same injection was given after L5 SNL-induced mechanical hyperalgesia had been established, MK-801 reversed the PWT reduction for 30-75 min, whereas NBQX, DL-AP3, or APDC had no effect. These results suggest that the manipulation of the peripheral Glu receptors reduces neuropathic pain, by blocking NMDA and group-I mGlu receptors and by stimulating group-II mGlu receptor during the induction phase of neuropathic pain, but only by blocking the NMDA receptor during its maintenance phase.

Authors+Show Affiliations

Department of Physiology, Yonsei University College of Medicine, C.P.O. Box 8044, Seoul, 120-752, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15450364

Citation

Jang, J H., et al. "Peripheral Glutamate Receptors Contribute to Mechanical Hyperalgesia in a Neuropathic Pain Model of the Rat." Neuroscience, vol. 128, no. 1, 2004, pp. 169-76.
Jang JH, Kim DW, Sang Nam T, et al. Peripheral glutamate receptors contribute to mechanical hyperalgesia in a neuropathic pain model of the rat. Neuroscience. 2004;128(1):169-76.
Jang, J. H., Kim, D. W., Sang Nam, T., Se Paik, K., & Leem, J. W. (2004). Peripheral glutamate receptors contribute to mechanical hyperalgesia in a neuropathic pain model of the rat. Neuroscience, 128(1), 169-76.
Jang JH, et al. Peripheral Glutamate Receptors Contribute to Mechanical Hyperalgesia in a Neuropathic Pain Model of the Rat. Neuroscience. 2004;128(1):169-76. PubMed PMID: 15450364.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Peripheral glutamate receptors contribute to mechanical hyperalgesia in a neuropathic pain model of the rat. AU - Jang,J H, AU - Kim,D-W, AU - Sang Nam,T, AU - Se Paik,K, AU - Leem,J W, PY - 2004/06/05/accepted PY - 2004/9/29/pubmed PY - 2004/11/17/medline PY - 2004/9/29/entrez SP - 169 EP - 76 JF - Neuroscience JO - Neuroscience VL - 128 IS - 1 N2 - We hypothesized that glutamate (Glu) released from the peripheral terminals of primary afferents contributes to the generation of mechanical hyperalgesia following peripheral nerve injury. Nerve injury was performed on rats with a lumbar 5 spinal nerve lesion (L5 SNL), which was preceded by L5 dorsal rhizotomy (L5 DR) to avoid the potential central effects induced by L5 SNL through the L5 dorsal root. Mechanical hyperalgesia, as evidenced by a reduction in paw withdrawal threshold (PWT), was short-lasting (<6 days) after L5 DR, but persistent (>42 days) after L5 SNL preceded by L5 DR. When an intraplantar injection into the affected hind paw was given immediately before L5 SNL, non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 (20 nmol), group-I metabotropic Glu (mGlu) receptor antagonist DL-amino-3-phosphonopropionic acid (DL-AP3; 70 nmol), and selective group-II mGlu receptor agonist 4-aminopyrrolidine-2,4-dicarboxylate (APDC; 20 nmol) delayed the onset of PWT reduction for 1-4 days. However, this onset was not affected by alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid/kainate receptor antagonist 2,3-dioxo-6-nitro-1,2,3,4,-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX; 100 nmol). When the same injection was given after L5 SNL-induced mechanical hyperalgesia had been established, MK-801 reversed the PWT reduction for 30-75 min, whereas NBQX, DL-AP3, or APDC had no effect. These results suggest that the manipulation of the peripheral Glu receptors reduces neuropathic pain, by blocking NMDA and group-I mGlu receptors and by stimulating group-II mGlu receptor during the induction phase of neuropathic pain, but only by blocking the NMDA receptor during its maintenance phase. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/15450364/Peripheral_glutamate_receptors_contribute_to_mechanical_hyperalgesia_in_a_neuropathic_pain_model_of_the_rat_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(04)00477-4 DB - PRIME DP - Unbound Medicine ER -