Impaired recovery of noradrenaline levels in apolipoprotein E-deficient mice after N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine lesion.
We investigated the effect of the noradrenergic neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP-4) (1 or 3 x 50 mg/kg, intraperitoneally), on hippocampal, cortical and cerebellar noradrenaline levels after recovery of one, five and 11 months in control and apolipoprotein E-deficient mice. Apolipoprotein E-deficient mice had lower hippocampal noradrenaline levels than control mice. DSP-4-lesioned control mice had a more extensive recovery of hippocampal and cortical noradrenaline levels than DSP-4-lesioned apoE-deficient mice after five months' survival. Furthermore, the hippocampal noradrenaline levels after five and 11 months and cortical noradrenaline levels after five months of recovery had slightly recovered in control but not in apolipoprotein E-deficient mice treated with a single dose of DSP-4 compared with mice treated with three doses of DSP-4. These results show that apolipoprotein E-deficient mice have impaired recovery capacity in their locus coeruleus neurons.[1]References
- Impaired recovery of noradrenaline levels in apolipoprotein E-deficient mice after N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine lesion. Puoliväli, J., Pradier, L., Riekkinen, P. Neuroscience (2000) [Pubmed]
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