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Titolo:
Nicotinic acetylcholine receptors in neonatal motoneurons are regulated byaxotomy: An electrophysiological and immunohistochemical study in human bcl-2 transgenic mice
Autore:
Zaninetti, M; Dubois-Dauphin, M; Lindstrom, J; Raggenbass, M;
Indirizzi:
Univ Geneva, Med Ctr, Dept Physiol, CH-1211 Geneva 4, Switzerland Univ Geneva Geneva Switzerland 4 Physiol, CH-1211 Geneva 4, Switzerland Univ Hosp Geneva, Div Neuropsychiat, CH-1225 Geneva, Switzerland Univ HospGeneva Geneva Switzerland CH-1225 CH-1225 Geneva, Switzerland Univ Penn, Sch Med, Dept Neurosci, Philadelphia, PA 19104 USA Univ Penn Philadelphia PA USA 19104 Neurosci, Philadelphia, PA 19104 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 3, volume: 100, anno: 2000,
pagine: 589 - 597
SICI:
0306-4522(2000)100:3<589:NARINM>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACIAL MOTONEURONS; ALZHEIMERS-DISEASE; ALPHA-7 RECEPTOR; TEMPORAL CORTEX; CELL-DEATH; BRAIN; SUBUNITS; METHYLLYCACONITINE; PROTOONCOGENE; NEURONS;
Keywords:
dihydro-beta-erythroidine; facial nucleus; mcthyllycaconitine; motoneuron degeneration; whole cell recordings;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Raggenbass, M Univ Geneva, Med Ctr, Dept Physiol, CH-1211 Geneva 4, Switzerland Univ Geneva Geneva Switzerland 4 211 Geneva 4, Switzerland
Citazione:
M. Zaninetti et al., "Nicotinic acetylcholine receptors in neonatal motoneurons are regulated byaxotomy: An electrophysiological and immunohistochemical study in human bcl-2 transgenic mice", NEUROSCIENC, 100(3), 2000, pp. 589-597

Abstract

Motoneuron axotomy was exploited as a model system for studying functionaland morphological changes caused in motoneuron cell bodies by peripheral axon injury. Rodent facial motoneurons express functional nicotinic acetylcholine receptors. We have determined the effect of neonatal unilateral facial nerve transection on these receptors by using electrophysiological and immunohistochemical techniques. To avoid rapid apoptotic cell death of axotomized motoneurons, the study was done in mice overexpressing the human bcl-2transgene. Intact motoneurons responded to acetylcholine by generating a rapidly rising inward current, which was insensitive to methyllycaconitine, a selective antagonist of alpha7-containing nicotinic receptors, bur was suppressed by dihydro-beta -erythroidine, a broad-spectrum antagonist. This indicates that mouse facial motoneurons possess nicotinic receptors which art: probably devoid of the alpha7 subunit. In striking contrast, axotomized motoneurons displayed little or no sensitivity to acetylcholine. Axotomy did not affect the sensitivity of facial motoneurons to the selective glutamate receptor agonist alpha -arnino-3-hydroxy-5-methyl-5-isoxaxolepropionic acid. Immunohistochemical studies revealed that the alpha4 nicotinic receptor subunit was present in intact motoneurons but was undetectable in axotomized motoneurons. By contrast, the beta2 subunit was comparable in intact and axotomized motoneurons. alpha3 immunoreactivity was undetectable, both inintact and in axotomized motoneurons. Thus, mouse facial nicotinic receptors are possibly of the alpha4 beta2 type and axotomy interferes negatively with the expression of the alpha4 subunit. By down-regulating nicotinic receptors, peripheral nerve injury may facilitate motoneuron degeneration. Alternatively, nicotinic receptor downregulation and motoneuron degeneration may be independent consequences of peripheral axotomy. (C) 2000 IBRO. Published by Elsevier Science Ltd. All rights reserved.

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Documento generato il 13/07/20 alle ore 10:46:24