Moderate cortical EEG changes in apolipoprotein E-deficient mice during ageing and scopolamine treatment but not after nucleus basalis lesion

Rationale: Recent studies suggest that apoE-deficient mice may have impaire d central cholinergic function and neuronal recovery capacity. Objective: W e investigated whether apoE-deficient mice an more susceptible to the bioch emical and EEG defects induced by ageing or nucleus basalis (NB) lesion. Me thods: ApoE-deficient and control mice were used. The baseline EEG activity and EEG response to a muscarinic acetylcholine receptor antagonist, scopol amine (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 EE G activity and EEG response to scopolamine (0.05 and 0.2 mg/kg), and cortic al ChAT activity, were studied after quisqualic acid-induced unilateral NE lesion. Results: The baseline EEG fast wave activity (relative alpha and be ta) was higher in apoE-deficient mice. Ageing decreased relative alpha acti vity similarly in both strains. The scopolamine induced EEG slowing was les s prominent in apoE-deficient than in control mice, and the difference betw een the strains became slightly clearer during ageing. The NB lesion failed to produce more severe changes in cortical EEG and ChAT activity in apoE-d eficient mice. Cortical and hippocampal ChAT activity was equal in young an d aged apoE-deficient and control mice. The EEG response to diazepam in you ng and aged mice was similar in both strains. Conclusions: The regulation o f 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.