Neurotrophin effects on survival and expression of cholinergic properties in cultured rat septal neurons under normal and stress conditions

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38 Scopus citations

Abstract

These studies tested the hypothesis that survival-promoting effects of neurotrophins on basal forebrain cholinergic neurons are enhanced under stress. Septal neurons from embryonic day 14-15 rats exposed for 10-14 d to neurotrophin [nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), or neurotrophin-4 (NT-4), each at 100 ng/ml] showed a two- to threefold increase in choline acetyltransferase (CHAT) activity, with little evidence of synergistic interactions. Neurotrophins produced no significant increase in the survival of total or acetylcholinesterase (AChE)-positive neurons at moderate plating density (1200-1600 cells/mm2). However, with very low plating densities (2-28 cells/mm2) BDNF, NT-3, and NT-4 (but not NGF) increased total neuronal survival, and BDNF increased survival of AChE-positive neurons. NGF and BDNF enhanced ChAT activity and survival of cholinergic neurons after a 24 hr hypoglycemic stress, even when added 1 hr after stress onset. All four tested neurotrophins increased total neuronal survival after hypoglycemic stress. These results suggest that neurotrophins are important for preservation of central cholinergic function under stress conditions, with different neurotrophins protecting against different stresses. The stress-associated survival-promoting effects of neurotrophins were not limited to the cholinergic subpopulation.

Original languageEnglish (US)
Pages (from-to)6665-6675
Number of pages11
JournalJournal of Neuroscience
Volume16
Issue number21
DOIs
StatePublished - Nov 1 1996

Keywords

  • basal forebrain
  • brain-derived neurotrophic factor
  • central cholinergic neurons
  • choline acetyltransferase
  • hypoglycemia
  • nerve growth factor
  • neuronal survival
  • neurotrophin- 4
  • neurotrophin-3
  • neurotrophins
  • septum
  • stress protection

ASJC Scopus subject areas

  • Neuroscience(all)

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