Journal of Neural Transmission

, Volume 113, Issue 7, pp 813–820

Chronic alcohol intoxication in rats leads to a strong but transient increase in NGF levels in distinct brain regions

Authors

  • C. A. Gericke
    • Institute of Health SciencesBerlin University of Technology
  • O. Schulte-Herbrüggen
    • Department of NeurologyCharité-University Medicine Berlin, Campus Benjamin Franklin, Humboldt-University and Free University of Berlin
  • T. Arendt
    • Paul Flechsig Institute of Brain Research, Department of NeuroanatomyUniversity of Leipzig
  • R. Hellweg
    • Department of Psychiatry and PsychotherapyCharité-University Medicine Berlin, Campus Benjamin Franklin, Humboldt-University and Free University of Berlin
Article

DOI: 10.1007/s00702-005-0361-x

Cite this article as:
Gericke, C., Schulte-Herbrüggen, O., Arendt, T. et al. J Neural Transm (2006) 113: 813. doi:10.1007/s00702-005-0361-x

Summary.

Nerve growth factor (NGF), a member of the neurotrophin family, is an essential mediator of neuronal activity and synaptic plasticity of basal forebrain cholinergic neurons. In this study NGF-protein levels were determined in areas of the basal forebrain cholinergic system, its projection areas as well as the striatum and the cerebellum after long-term exposure (6 and 9 months) to ethanol and a phase of withdrawal in male Sprague-Dawley rats. 6-month alcohol treatment led to an increase of NGF to 650–850% of controls in the basal forebrain and the septum and to a 210–485% increase in the cholinergic projection areas (anterior cortex, hippocampus and olfactory bulb). After 9 months exposure to ethanol, a decrease of NGF by 16% in the frontal cortex was observed compared to controls. In the other brain regions no differences in NGF expression were detectable at this time-point. These results support the idea of an endogenous neuroprotective mechanism acting through a transient NGF induction followed by a decrease in NGF-levels during the course of further neuronal degeneration.

Keywords: NGF, basal forebrain, cholinergic degeneration, ethanol.

Copyright information

© Springer-Verlag 2005