Skip to Main Content (Press Enter)

Logo CNR
  • ×
  • Home
  • Persone
  • Pubblicazioni
  • Strutture
  • Competenze

UNI-FIND
Logo CNR

|

UNI-FIND

cnr.it
  • ×
  • Home
  • Persone
  • Pubblicazioni
  • Strutture
  • Competenze
  1. Pubblicazioni

The effect of long-term alcohol intake on brain NGF-targe cells of aged rats

Articolo
Data di Pubblicazione:
1992
Abstract:
It was reported that chronic exposure to ethanol causes a loss of hippocampal pyramidal cells and of brain cholinergic neurons in both laboratory animals and humans. In the present study, it was hypothesized that nerve growth factor (NGF), a trophic agent for the survival and maintenance of basal forebrain cholinergic neurons (FCN), might be affected by the neurodegenerative events which occur during ethanol consumption. To test this hypothesis, we used aged rats (14 months) exposed for 16 weeks to 40 g/kg per day of undiluted wine. Our experiments showed that chronic alcohol consumption causes a reduction of NGF in the hippocampus (HI) and of choline acetyltransferase (ChAT) activity in both the septum and the HI and a reduction in the distribution of NGF-receptors (NGF-R) in the septum and nucleus of Meynert. Intracerebral injection of NGF in alcohol-exposed rats results in a return to normal levels of ChAT enzymatic activity and NGF-R expression. These experiments indicate that the damaging effect of alcohol on the FCN is also associated with impairment of central NGF-target structures. © 1992.
Tipologia CRIS:
01.01 Articolo in rivista
Keywords:
Aged rats; Alcohol; Choline acetyltransferase; Cholinergic neurons; Nerve growth factor
Elenco autori:
Tirassa, Paola
Autori di Ateneo:
TIRASSA PAOLA
Link alla scheda completa:
https://iris.cnr.it/handle/20.500.14243/307504
Pubblicato in:
ALCOHOL (FAYETTEVILLE, N.Y.)
Journal
  • Dati Generali

Dati Generali

URL

http://www.scopus.com/record/display.url?eid=2-s2.0-0026681483&origin=inward
  • Utilizzo dei cookie

Realizzato con VIVO | Designed by Cineca | 26.5.0.0 | Sorgente dati: PREPROD (Ribaltamento disabilitato)