Characterization of the glutamatergic system for induction and maintenance of allodynia

Autor: Toshiaki Minami, Kenji Sakimura, Emiko Okuda-Ashitaka, Seiji Ito, Hidemaro Mori, Keiko Shimamoto, Masayoshi Mishina, Shinji Matsumura
Rok vydání: 2001
Předmět:
Male
N-Methylaspartate
Amino Acid Transport System X-AG
Glutamic Acid
Pain
Kainate receptor
AMPA receptor
Pharmacology
Dinoprost
Synaptic Transmission
Dinoprostone
Mice
chemistry.chemical_compound
Glutamatergic
Physical Stimulation
Excitatory Amino Acid Agonists
medicine
Animals
Excitatory Amino Acid Agonist
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid
Molecular Biology
Pain Measurement
Mice
Knockout
Aspartic Acid
Chemistry
musculoskeletal
neural
and ocular physiology
General Neuroscience
Glutamate receptor
Glutamic acid
Mice
Inbred C57BL
Posterior Horn Cells
Allodynia
Animals
Newborn
Receptors
Glutamate
nervous system
Biochemistry
Touch
Synapses
NMDA receptor
ATP-Binding Cassette Transporters
lipids (amino acids
peptides
and proteins)
Neurology (clinical)
Capsaicin
medicine.symptom
Developmental Biology
Zdroj: Brain Research. 895:178-185
ISSN: 0006-8993
Popis: Glutamate is the main excitatory neurotransmitter in the central nervous system and has been shown to be involved in spinal nociceptive processing. We previously demonstrated that intrathecal (i.t.) administration of prostaglandin (PG) E(2) and PGF(2 alpha) induced touch-evoked pain (allodynia) through the glutamatergic system by different mechanisms. In the present study, we characterized glutamate receptor subtypes and glutamate transporters involved in induction and maintenance of PGE(2)- and PGF(2 alpha)-evoked allodynia. In addition to PGE(2) and PGF(2 alpha), N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), but not kainate, induced allodynia. PGE(2)- and NMDA-induced allodynia were observed in NMDA receptor epsilon 4 (NR2D) subunit knockout (GluR epsilon 4(-/-)) mice, but not in epsilon 1 (NR2A) subunit knockout (GluR epsilon 1(-/-)) mice. Conversely, PGF(2 alpha)- and AMPA-induced allodynia were observed in GluR epsilon 1(-/-) mice, but not in GluR epsilon 4(-/-) mice. The induction of allodynia by PGE(2) and NMDA was abolished by the NMDA receptor epsilon 2 (NR2B) antagonist CP-101,606 and neonatal capsaicin treatment. PGF(2 alpha)- and AMPA-induced allodynia were not affected by CP-101,606 and by neonatal capsaicin treatment. On the other hand, the glutamate transporter blocker DL-threo-beta-benzyloxyaspartate (DL-TBOA) blocked all the allodynia induced by PGE(2), PGF(2 alpha), NMDA, and AMPA. These results demonstrate that there are two pathways for induction of allodynia mediated by the glutamatergic system and suggest that the glutamate transporter is essential for the induction and maintenance of allodynia.
Databáze: OpenAIRE
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