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Titolo:
Contribution of alpha(2) receptor subtypes to nerve injury-induced pain and its regulation by dexmedetomidine
Autore:
Malmberg, AB; Hedley, LR; Jasper, JR; Hunter, JC; Basbaum, AI;
Indirizzi:
Univ Calif San Francisco, WM Keck Ctr Integrat Neurosci, Dept Anat, San Francisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Univ Calif San Francisco, WM Keck Ctr Integrat Neurosci, Dept Physiol, SanFrancisco, CA 94143 USA Univ Calif San Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Roche Biosci, Neurobiol Unit, Palo Alto, CA 94304 USA Roche Biosci Palo Alto CA USA 94304 urobiol Unit, Palo Alto, CA 94304 USA
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 8, volume: 132, anno: 2001,
pagine: 1827 - 1836
SICI:
0007-1188(200104)132:8<1827:COARST>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
DORSAL-ROOT GANGLION; RAT SPINAL-CORD; SYMPATHETICALLY MAINTAINED PAIN; PRIMARY AFFERENT NEURONS; NEUROPATHIC PAIN; MECHANICAL ALLODYNIA; SUBSTANCE-P; ALPHA(2)-ADRENOCEPTOR SUBTYPES; ALPHA(2A)-ADRENERGIC RECEPTOR; ADRENERGIC SENSITIVITY;
Keywords:
alpha adrenergic receptors; peripheral nerve injury; neuropathic pain; thermal and mechanical allodynia; antinociception; guanethidine sympathectomy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Malmberg, AB NeurogesX Inc, 969C Ind Rd, San Carlos, CA 94070 USA NeurogesX Inc 969C Ind Rd San Carlos CA USA 94070 A 94070 USA
Citazione:
A.B. Malmberg et al., "Contribution of alpha(2) receptor subtypes to nerve injury-induced pain and its regulation by dexmedetomidine", BR J PHARM, 132(8), 2001, pp. 1827-1836

Abstract

1 There is evidence that noradrenaline contributes to the development and maintenance of neuropathic pain produced by trauma to a peripheral nerve. It is, however, unclear which subtype(s) of alpha adrenergic receptors (AR) may be involved. In addition to pro-nociceptive actions of AR stimulation, alpha (2) AR agonists produce antinociceptive effects.2 Here we studied the contribution of the alpha (2) AR subtypes, alpha (2A), alpha (2B) and alpha (2C) to the development of neuropathic pain. We also examined the antinociceptive effect produced by the alpha (2) AR agonist dexmedetomidine in nerve-injured mice.3 The studies were performed in mice that carry either a point (alpha (2A)) or a null (alpha (2B) and alpha (2C)) mutation in the gene encoding the alpha (2) AR. To induce a neuropathic pain condition, we partially ligated the sciatic nerve and measured changes in thermal and mechanical sensitivity.4 Baseline mechanical and thermal withdrawal thresholds were similar in all mutant and wild-type mice; and, after peripheral nerve injury, all mice developed comparable hypersensitivity (allodynia) to thermal and mechanical stimulation.5 Dexmedetomidine reversed the allodynia at a low dose (3 mug kg(-1), s.c.) and produced antinociceptive effects at higher doses (10-30 mug kg(-1)) in all groups except in alpha (2A) AR mutant mice. The effect of dexmedetomidine was reversed by intrathecal, but not systemic, injection of the alpha (2) AR antagonist RS 42206.6 These results suggest that neither alpha (2A), alpha (2B) nor alpha (2C)AR is required for the development of neuropathic pain after peripheral nerve injury, however, the spinal alpha (2A) AR is essential for the antinociceptive effects of dexmedetomidine.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/01/21 alle ore 08:27:15