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Titolo:
Neuronal plasticity and signal transduction in nociceptive neurons: Implications for the initiation and maintenance of pathological pain
Autore:
Ji, RR; Woolf, CJ;
Indirizzi:
Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Neural Plast Res Grp,Boston, MA 02114 USA Massachusetts Gen Hosp Boston MA USA 02114 t Res Grp,Boston, MA 02114 USA Harvard Univ, Sch Med, Boston, MA 02129 USA Harvard Univ Boston MA USA 02129 vard Univ, Sch Med, Boston, MA 02129 USA
Titolo Testata:
NEUROBIOLOGY OF DISEASE
fascicolo: 1, volume: 8, anno: 2001,
pagine: 1 - 10
SICI:
0969-9961(200102)8:1<1:NPASTI>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; DORSAL-ROOT GANGLIA; RAT SPINAL-CORD; NITRIC-OXIDE SYNTHASE; TRANSCRIPTION FACTOR CREB; RECEPTOR MESSENGER-RNA; C-FOS TRANSCRIPTION; NEUROPATHIC PAIN; SENSORY NEURONS; INFLAMMATORY PAIN;
Keywords:
pathological pain; MAP kinase; nociceptive neurons; spinal cord; primary sensory neurons; central sensitization; neuronal plasticity; signal transduction; transcription;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
91
Recensione:
Indirizzi per estratti:
Indirizzo: Ji, RR Massachusetts Gen Hosp, Dept Anesthesia & Crit Care, Neural Plast Res Grp,Boston, MA 02114 USA Massachusetts Gen Hosp Boston MA USA 02114 rp,Boston, MA 02114 USA
Citazione:
R.R. Ji e C.J. Woolf, "Neuronal plasticity and signal transduction in nociceptive neurons: Implications for the initiation and maintenance of pathological pain", NEUROBIOL D, 8(1), 2001, pp. 1-10

Abstract

Pathological pain, consisting of tissue injury-induced inflammatory and nerve injury-induced neuropathic pain, is an expression of neuronal plasticity. One component of this is that the afferent input generated by injury andintense noxious stimuli triggers an increased excitability of nociceptive neurons in the spinal cord. This central sensitization is an activity-dependent functional plasticity that results from activation of different intracellular kinase cascades leading to the phosphorylation of key membrane receptors and channels, increasing synaptic efficacy. Central sensitization is both induced and maintained in a transcription-independent manner. Several different intracellular signal transduction cascades converge on MAPK (mitogen-activated protein kinase), activation of which appears to be a master switch or gate for the regulation of central sensitization. In addition to posttranslational regulation, the MAPK pathway may also regulate long-term pain hypersensitivity, via transcriptional regulation of key gene products. Pharmacological intervention targeted specifically at the signal transduction pathways in nociceptive neurons may provide, therefore, new therapeutic opportunities for pathological pain. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 17:16:28