title: Moderate cortical EEG changes in apolipoprotein E-deficient mice during ageing and scopolamine treatment but not after nucleus basalis lesion.
abstract: BACKGROUND
  Recent studies suggest that apoE-deficient mice may have impaired central cholinergic function and neuronal recovery capacity.
  
  
  OBJECTIVE
  We investigated whether apoE-deficient mice are more susceptible to the biochemical and EEG defects induced by ageing or nucleus basalis (NB) lesion.
  
  
  METHODS
  ApoE-deficient and control mice were used. The baseline EEG activity and EEG response to a muscarinic acetylcholine receptor antagonist, scopolamine (0.05 and 0.2 mg/kg) and a benzodiazepine receptor agonist, diazepam (0.5 and 2.0 mg/kg), were studied during ageing. In addition, the cortical and hippocampal ChAT activities were measured in aged mice. The baseline EEG activity and EEG response to scopolamine (0.05 and 0.2 mg/kg), and cortical ChAT activity, were studied after quisqualic acid-induced unilateral NB lesion.
  
  
  RESULTS
  The baseline EEG fast wave activity (relative alpha and beta) was higher in apoE-deficient mice. Ageing decreased relative alpha activity similarly in both strains. The scopolamine induced EEG slowing was less prominent in apoE-deficient than in control mice, and the difference between the strains became slightly clearer during ageing. The NB lesion failed to produce more severe changes in cortical EEG and ChAT activity in apoE-deficient mice. Cortical and hippocampal ChAT activity was equal in young and aged apoE-deficient and control mice. The EEG response to diazepam in young and aged mice was similar in both strains.
  
  
  CONCLUSIONS
  The regulation of cortical EEG activity of apoE-deficient mice was somewhat altered during ageing and the response to scopolamine treatment was blunted. However, the cholinergic cells of the NB of apoE-deficient mice were not more sensitive to lesion or to ageing, suggesting that apoE does not have to be present to preserve the viability of cholinergic neurons.
authors.affiliation: Department of Neuroscience and Neurology, University of Kuopio and Kuopio University Hospital, P.O. Box 1627, FIN-70211 Kuopio, Finland. jukka.puolivali@uku.fi
authors.forename: J
authors.initials: J
authors.lastname: Puoliväli
authors.forename: L
authors.initials: L
authors.lastname: Pradier
authors.forename: P
authors.initials: P
authors.lastname: Riekkinen
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency*; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D003975:Diazepam / Q000494:pharmacology; D004569:Electroencephalography / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016548:Prosencephalon / Q000502:physiology*; D012601:Scopolamine / Q000494:pharmacology*
chemical_list: D001057:Apolipoproteins E; D012601:Scopolamine; D002795:Choline O-Acetyltransferase; D003975:Diazepam