Traumatic brain injury reduces hippocampal high-affinity [3H]choline uptake but not extracellular choline levels in rats.
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.
Dixon
C E
CE
Department of Neurosurgery, University of Texas, Houston 77030.
Bao
J
J
Bergmann
J S
JS
Johnson
K M
KM
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
D002794:Choline; D000109:Acetylcholine