Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Nerve growth factor (NGF) augments cortical and hippocampal cholinergic functioning after p75NGF receptor-mediated deafferentation but impairs inhibitory avoidance and induces fear-related behaviors
Autore:
Winkler, J; Ramirez, GA; Thal, LJ; Waite, JJ;
Indirizzi:
Univ Calif San Diego, Dept Neurosci, La Jolla, CA 92093 USA Univ Calif SanDiego La Jolla CA USA 92093 urosci, La Jolla, CA 92093 USA Vet Affairs Med Ctr San Diego, Neurol Serv, La Jolla, CA 92161 USA Vet Affairs Med Ctr San Diego La Jolla CA USA 92161 a Jolla, CA 92161 USA Univ Regensburg, Dept Neurol, D-93053 Regensburg, Germany Univ RegensburgRegensburg Germany D-93053 , D-93053 Regensburg, Germany
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 2, volume: 20, anno: 2000,
pagine: 834 - 844
SICI:
0270-6474(20000115)20:2<834:NGF(AC>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEUS BASALIS MAGNOCELLULARIS; RIBOSOME-INACTIVATING PROTEINS; ALZHEIMERS-DISEASE; ACOUSTIC STARTLE; QUISQUALIC ACID; LESIONED RATS; INTRACEREBROVENTRICULAR INFUSION; ACETYLCHOLINE SYNTHESIS; SPATIAL MEMORY; IBOTENIC ACID;
Keywords:
basal forebrain; immunotoxin; 192IgG-saporin; NGF; water maze; inhibitory avoidance; startle response; choline acetyltransferase; low-affinity nerve growth factor receptor;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Waite, JJ Univ Calif San Diego, Dept Neurosci 9151, 3350 La Jolla Village Dr, La Jolla, CA 92161 USA Univ Calif San Diego 3350 La Jolla Village Dr LaJolla CA USA 92161
Citazione:
J. Winkler et al., "Nerve growth factor (NGF) augments cortical and hippocampal cholinergic functioning after p75NGF receptor-mediated deafferentation but impairs inhibitory avoidance and induces fear-related behaviors", J NEUROSC, 20(2), 2000, pp. 834-844

Abstract

Nerve growth factor (NGF) enhances cholinergic functioning in animals witha compromised cholinergic basal forebrain (CBF). Immunotoxic lesions targeting low-affinity NGF receptor (p75NGF receptor)-bearing CBF neurons provide a selective model for testing the effects of NGF on residual cholinergic neurons. Rats received PBS or the immunotoxin 192IgG-saporin (192Sap) intracerebroventricularly at two doses (1 or 2.7 mu g) known to produce different degrees of cholinergic deficit. Seven weeks after lesioning, half of eachgroup received either NGF or cytochrome c intracerebroventricularly for 7 weeks. The two doses of 192Sap produced 50 and 80% depletions of choline acetyltransferase (ChAT) activity in the neocortex and hippocampus. NGF produced the greatest increase in ChAT activity in controls, intermediate in low-lesioned, and smallest in highly lesioned animals. NGF-treated animals showed reduced weight gain, hyper-responsiveness to acoustic stimuli, and decreased inhibitory avoidance. Although general motor behavior was affected byneither 192Sap nor NGF in an open field task, highly lesioned rats took longer to reach the platform during water maze testing. Impaired spatial orientation in finding a hidden platform at the previously acquired position was mitigated by NGF. Hypertrophic changes of residual CBF neurons, Schwann cell hyperplasia, and aberrant axonal sprouting around the medulla were observed in NGF-treated animals only, independent of the preexisting lesion. Our results indicate that NGF has a limited capacity to enhance functioning of residual CBF neurons. More importantly, NGF augmented fear-related behaviors and adverse neuroproliferative changes that may restrict its therapeutic use.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 02:26:16