Spinal sensitization mechanism in vincristine-induced hyperalgesia in mice.
Neurosci Lett
; 343(2): 89-92, 2003 Jun 05.
Article
em En
| MEDLINE
| ID: mdl-12759171
ABSTRACT
Our aim was to investigate the possible involvement of spinal voltage-dependent Ca(2+) channels (VDCCs) in vincristine-induced hyperalgesia and also to characterize this hyperalgesic state in the spinal cord. Mice receiving vincristine displayed significantly lower mechanical nociceptive thresholds than controls. Intrathecal omega-conotoxin GVIA (an N-type blocker) produced dose-dependent inhibition of the mechanical nociception, its antinociceptive effect being greater in vincristine-treated mice than in controls. The antinociception of omega-agatoxin IVA (a P/Q-type blocker) and calciseptine (an L-type blocker) were both slightly, but not significantly greater in vincristine-treated mice. An N-methyl-D-aspartate-receptor antagonist but not a tachykinin-NK1-receptor antagonist produced greater antinociception in vincristine-treated mice. These results suggest that vincristine-induced hyperalgesia involves a sensitization of the spinal processing of mechanical sensory information via a mechanism involving N-type but not P/Q- or L-type VDCCs. A spinal glutamatergic pathway also appears to be involved in this hyperalgesia.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Medula Espinal
/
Valina
/
Vincristina
/
Hiperalgesia
Limite:
Animals
Idioma:
En
Ano de publicação:
2003
Tipo de documento:
Article