Dynorphin A increases substance P release from trigeminal primary afferent C-fibers.
Eur J Pharmacol
; 366(1): 27-34, 1999 Jan 29.
Article
em En
| MEDLINE
| ID: mdl-10064148
Dynorphin A-(1-17) has been found to produce spinal antianalgesia and allodynia. Thus, we studied whether dynorphin A-(1-17) modulates substance P release evoked by the C-fiber-selective stimulant capsaicin (1 microM) from trigeminal nucleus caudalis slices. Very low concentrations of dynorphin A-(1-17) (0.01-0.1 nM) strongly facilitated capsaicin-evoked substance P release. This dynorphin A-(1-17) effect was not blocked by the opioid receptor antagonists naloxone (100 nM), beta-funaltrexamine (20 nM), naloxonazine (1 nM), nor-binaltorphimine (3 nM) and ICI 174,864 (N,N-dialyl-Tyr-Aib-Phe-Leu; 0.3 microM). Yet, the effect of dynorphin A-(1-17) was blocked by the NMDA receptor antagonist MK-801 ((+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d] cyclohepten-5-10-imine maleate; 0.3 microM). Neonatal treatment with capsaicin (50 mg/kg s.c.), which destroys substance P-containing primary afferents, abolished the excitatory effect of dynorphin A-(1-17) on K+-evoked substance P release. In conclusion, dynorphin A-(1-17) increases substance P release from C-fibers by the activation of NMDA receptors which supports the involvement of presynaptic mechanisms in dynorphin-induced antianalgesia and allodynia.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Núcleos do Trigêmeo
/
Dinorfinas
/
Substância P
/
Fibras Nervosas
/
Neurônios Aferentes
Limite:
Animals
Idioma:
En
Revista:
Eur J Pharmacol
Ano de publicação:
1999
Tipo de documento:
Article
País de afiliação:
Venezuela
País de publicação:
Holanda