title: Traumatic brain injury reduces hippocampal high-affinity [3H]choline uptake but not extracellular choline levels in rats.
abstract: 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.
authors.affiliation: Department of Neurosurgery, University of Texas, Houston 77030.
authors.forename: C E
authors.initials: CE
authors.lastname: Dixon
authors.forename: J
authors.initials: J
authors.lastname: Bao
authors.forename: J S
authors.initials: JS
authors.lastname: Bergmann
authors.forename: K M
authors.initials: KM
authors.lastname: Johnson
mesh_terms: D000109:Acetylcholine / Q000096:biosynthesis; D000818:Animals; D001692:Biological Transport; D001930:Brain Injuries / Q000378:metabolism* / Q000523:psychology; D002794:Choline / Q000493:pharmacokinetics*; D003399:Craniotomy; D005110:Extracellular Space / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism*; D008569:Memory Disorders / Q000209:etiology / Q000503:physiopathology; D017551:Microdialysis; D009474:Neurons / Q000378:metabolism; D051381:Rats; D014949:Wounds, Nonpenetrating / Q000378:metabolism / Q000523:psychology
chemical_list: D002794:Choline; D000109:Acetylcholine