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Titolo:
Effect of IGF-I and neurotrophin-3 on gracile neuroaxonal dystrophy in diabetic and aging rats
Autore:
Schmidt, RE; Dorsey, DA; Beaudet, LN; Plurad, SB; Parvin, CA; Ohara, S;
Indirizzi:
Washington Univ, Sch Med, Dept Pathol, Div Neuropathol, St Louis, MO 63110USA Washington Univ St Louis MO USA 63110 Neuropathol, St Louis, MO 63110USA Washington Univ, Sch Med, Dept Pathol, Div Lab Med, St Louis, MO 63110 USAWashington Univ St Louis MO USA 63110 Div Lab Med, St Louis, MO 63110 USA Natl Chushin Matsumoto Hosp, Dept Neurol, Matsumoto, Nagano, Japan Natl Chushin Matsumoto Hosp Matsumoto Nagano Japan sumoto, Nagano, Japan
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1-2, volume: 876, anno: 2000,
pagine: 88 - 94
SICI:
0006-8993(20000908)876:1-2<88:EOIANO>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-I; SCIATIC-NERVE INJURY; NEUROPEPTIDE-Y RESPONSE; AGED RATS; AUTONOMIC GANGLIA; NEUROPATHY; REGENERATION; RECEPTOR; NUCLEUS; YOUNG;
Keywords:
neuropathy; sensory nervous system; medulla;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
23
Recensione:
Indirizzi per estratti:
Indirizzo: Schmidt, RE Washington Univ, Sch Med, Dept Pathol, Div Neuropathol, St Louis, MO 63110USA Washington Univ St Louis MO USA 63110 , St Louis, MO 63110USA
Citazione:
R.E. Schmidt et al., "Effect of IGF-I and neurotrophin-3 on gracile neuroaxonal dystrophy in diabetic and aging rats", BRAIN RES, 876(1-2), 2000, pp. 88-94

Abstract

Neuroaxonal dystrophy (NAD), a distinctive axonopathy characterized by dramatic swelling of preterminal axons and nerve terminals by the accumulationof a variety of subcellular organelles, develops in the central projections of sensory neurons to medullary gracile nuclei in aged animals and man, and in a number of diseases and experimental conditions. Although its pathogenesis is unknown, proposed mechanisms include abnormalities of axonal regeneration, collateral sprouting and synaptic plasticity which may reflect alteration in neurotrophic support. In the current study, we have demonstrated quantitatively that aging causes the expected marked increase in the frequency of gracile NAD; however, substantial numbers of dystrophic axons develop between 6 and 10 months of age, earlier than expected. Although diabetes has been reported to increase the frequency of NAD in the central processes of sensory neurons in the gracile fasciculus of genetically diabetic BE rats, we have found that 8-10 months of streptozotocin-induced diabetes results in fewer dystrophic axons in the gracile nucleus than in age-matched controls. Administration of neurotrophin-3 (NT-3) and insulin-like growth factor-I (IGF-I), which have been shown to affect synaptic plasticity (implicated in the pathogenesis of NAD), for the last two months before sacrifice did not affect the frequency of gracile NAD in controls or diabetics. The sensory terminals in the gracile nuclei provide a simple, well-characterizedexperimental system in which questions of pathogenesis and prevention of neuroaxonal dystrophy can be addressed. (C) 2000 Elsevier Science B.V. All rights reserved.

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Documento generato il 21/09/20 alle ore 08:58:34