Traumatic brain injury reduces hippocampal high-affinity [3H]choline uptake but not extracellular choline levels in rats

C. Edward Dixon, Juliang Bao, John S. Bergmann, Kenneth M. Johnson

Research output: Contribution to journalArticle

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Hippocampal cholinergic hypofunction may contribute to memory deficits following experimental traumatic brain injury. These studies examined two important factors in acetylcholine synthesis: choline availability and neuronal uptake. No reductions in basal extracellular choline levels, using microdialysis, were observed 2 weeks after cortical impact injury. However, studies of high affinity [3H]choline uptake in the hippocampus, measured in a synaptosomal preparation, found a reduction in the maximum velocity of choline uptake (Vmax), while no differences in affinity constants (Km) were found. The results suggest that post-traumatic cholinergic deficits are not attributable to decreased availability of choline, but may be associated with either a decreased ability of cholinergic neurons to take up choline and/or a loss of cholinergic neurons.

Original languageEnglish (US)
Pages (from-to)127-130
Number of pages4
JournalNeuroscience Letters
Issue number2
StatePublished - Oct 24 1994



  • Brain injury
  • Choline
  • High affinity choline uptake
  • Hippocampus
  • Microdialysis

ASJC Scopus subject areas

  • Neuroscience(all)

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