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Titolo:
Dynorphin A increases substance P release from trigeminal primary afferentC-fibers
Autore:
Arcaya, JL; Cano, G; Gomez, G; Maixner, W; Suarez-Roca, H;
Indirizzi:
Univezuela, Sch Med, Inst Invest Clin, Pharmacol Sect, Maracaibo 4001A, Ven Univ Zulia Maracaibo Venezuela 4001A harmacol Sect, Maracaibo 4001A, Ven Univ N Carolina, Dent Res Ctr, Chapel Hill, NC 27514 USA Univ N Carolina Chapel Hill NC USA 27514 s Ctr, Chapel Hill, NC 27514 USA
Titolo Testata:
EUROPEAN JOURNAL OF PHARMACOLOGY
fascicolo: 1, volume: 366, anno: 1999,
pagine: 27 - 34
SICI:
0014-2999(19990129)366:1<27:DAISPR>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
DORSAL HORN NEURONS; SPINAL-CORD; NMDA RECEPTOR; PERIPHERAL INFLAMMATION; IMMUNOHISTOCHEMICAL ANALYSIS; ANTIANALGESIC ACTION; OPIOID RECEPTORS; TRAUMATIC INJURY; NERVOUS-SYSTEM; NUCLEUS SLICES;
Keywords:
substance P; dynorphin; opioid receptor antagonist; NMDA receptor antagonist; primary afferent;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Suarez-Roca, H Univ,Zulia, Sch Med, Inst Invest Clin, Pharmacol Sect, Apartado Postal 1151 Univ Zulia Apartado Postal 1151 Maracaibo Venezuela 4001A
Citazione:
J.L. Arcaya et al., "Dynorphin A increases substance P release from trigeminal primary afferentC-fibers", EUR J PHARM, 366(1), 1999, pp. 27-34

Abstract

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 mu M) 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 mu M). 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 mu M) Neonatal treatment with capsaicin (50mg/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. (C) 1999 Elsevier Science B.V. All rights reserved.

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Documento generato il 10/04/20 alle ore 16:09:10