Evidence for the participation of peripheral 5-HT2A, 5-HT2B, and 5-HT2C receptors in formalin-induced secondary mechanical allodynia and hyperalgesia.
Neuroscience
; 232: 169-81, 2013 Mar 01.
Article
em En
| MEDLINE
| ID: mdl-23219842
The role of 5-HT2A/2B/2C receptors in formalin-induced secondary allodynia and hyperalgesia in rats was assessed. Formalin produced acute nociceptive behaviors (flinching and licking/lifting) followed by long-term secondary mechanical allodynia and hyperalgesia. Pre-treatment for five consecutive days with compound 48/80 (1, 3, 10, 10, and 10 µg/paw) prevented formalin-induced secondary allodynia and hyperalgesia. Ipsilateral, but not contralateral, peripheral pre-treatment (nmol/paw) with the 5-HT2 receptor agonist DOI (3-30), 5-HT (10-100) or fluoxetine (0.3-3) significantly increased 0.5% formalin-induced secondary allodynia and hyperalgesia in both paws. The pronociceptive effect of DOI (10 nmol/paw), 5-HT (100 nmol/paw) and fluoxetine (1 nmol/paw) was blocked by selective 5-HT2A (ketanserin), 5-HT2B (RS-127445), and 5-HT2C (RS-102221) receptor antagonists. Furthermore, ipsilateral pre-treatment (nmol/paw) with ketanserin (1, 10, and 100), RS-127445 (0.01, 0.1 and 1) or RS-102221 (1, 10 and 100) prevented while post-treatment reversed 1% formalin-induced secondary allodynia and hyperalgesia in both paws. In marked contrast, contralateral injection of the greatest tested dose of 5-HT2A/2B/2C receptor antagonists did not modify long-lasting secondary allodynia and hyperalgesia. These results suggest that 5-HT released from mast cells after formalin injection sensitizes primary afferent neurons via 5-HT2A/2B/2C receptors leading to the development and maintenance of secondary allodynia and hyperalgesia.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Receptor 5-HT2A de Serotonina
/
Receptor 5-HT2B de Serotonina
/
Receptor 5-HT2C de Serotonina
/
Formaldeído
/
Hiperalgesia
Limite:
Animals
Idioma:
En
Revista:
Neuroscience
Ano de publicação:
2013
Tipo de documento:
Article
País de afiliação:
México
País de publicação:
Estados Unidos