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Titolo:
Effects of amyloid peptides on cell viability and expression of neuropeptides in cultured rat dorsal root ganglion neurons: a role for free radicals and protein kinase C
Autore:
Ma, WY; Zheng, WH; Belanger, S; Kar, S; Quirion, R;
Indirizzi:
McGill Univ, Douglas Hosp, Res Ctr, Verdun, PQ H4H 1R3, Canada McGill Univ Verdun PQ Canada H4H 1R3 Res Ctr, Verdun, PQ H4H 1R3, Canada McGill Univ, Dept Psychiat, Verdun, PQ H4H 1R3, Canada McGill Univ VerdunPQ Canada H4H 1R3 Psychiat, Verdun, PQ H4H 1R3, Canada
Titolo Testata:
EUROPEAN JOURNAL OF NEUROSCIENCE
fascicolo: 6, volume: 13, anno: 2001,
pagine: 1125 - 1135
SICI:
0953-816X(200103)13:6<1125:EOAPOC>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
GENE-RELATED PEPTIDE; SCIATIC-NERVE INJURY; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; SPINAL-CORD; BETA-PROTEIN; SENSORY NEURONS; PERIPHERAL-NERVE; AGED RATS; CALCIUM HOMEOSTASIS;
Keywords:
calcitonin gene-related peptide; galanin; immunocytochemistry; neuropeptide Y; superoxide dismutase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
67
Recensione:
Indirizzi per estratti:
Indirizzo: Quirion, R McGill Univ, Douglas Hosp, Res Ctr, 6875 Boul LaSalle, Verdun, PQ H4H 1R3,Canada McGill Univ 6875 Boul LaSalle Verdun PQ Canada H4H 1R3 3,Canada
Citazione:
W.Y. Ma et al., "Effects of amyloid peptides on cell viability and expression of neuropeptides in cultured rat dorsal root ganglion neurons: a role for free radicals and protein kinase C", EUR J NEURO, 13(6), 2001, pp. 1125-1135

Abstract

Chronic pain caused by nerve injury and inflammation is more common in theelderly. However, mechanisms underlying this phenomenon are unclear. Higher sensitivity of sensory neurons to free radicals has been suggested as onepossibility. The production of free radicals can be induced by various agents, including the highly toxic protein beta -amyloid (A beta), which is found in higher amounts in the brains of Alzheimer's Disease patients. In dorsal root ganglion (DRG) cultures exposed to A beta, we examined cellular toxicity and peptide expression, in particular calcitonin gene-related peptide (CGRP), a peptide which is abundantly expressed by nociceptive afferents and is known to be involved in pain processes. Exposure of cultured rat DRGneurons to A beta (25-35) or A beta (1-40) (10 or 20 mum for 24-96 h) increased trypan blue-stained cells in a concentration- and time-dependent manner, thus, indicating cellular toxicity. These treatments also increased thenumber of CGRP immunoreactive (IR) neurons while decreasing the number of neuropeptide Y- and galanin-IR neurons. The free radical scavenger, superoxide dismutase, attenuated both the toxicity and neuropeptide changes induced by A beta, thus, suggesting that oxidative stress probably contributes tothese effects. Exposure of cultured DRG neurons to A beta also increased the number of protein kinase C alpha (PKC alpha)-IR neurons. The PKC inhibitors, chelerythrine chloride and Go6976, significantly augmented A beta -induced cellular toxicity while attenuating the increases in CGRP-and PKC alpha -IR cells, supporting the notion of a protective role for PKC in A beta insults. These in vitro data suggest that A beta peptides may, in addition to causing neurotoxicity, regulate neuropeptide expression in primary afferents. This finding could be relevant to the higher incidence of neuropathic pain that occurs with ageing.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 20:53:27