Apolipoprotein D (ApoD) has many actions critical to maintaining mammalian CNS function. It is therefore
significant that levels of ApoD have been shown to be altered in the CNS of subjects with schizophrenia,
suggesting a role for ApoD in the pathophysiology of the disorder. There is also a large body of evidence that
cortical and hippocampal glutamatergic, serotonergic and cholinergic systems are affected by the pathophysiology
of schizophrenia. Thus, we decided to use in vitro radioligand binding and autoradiography tomeasure levels
of ionotropic glutamate, somemuscarinic and serotonin 2Areceptors in theCNS ofApoD-/- and isogenic wild-type
mice. These studies revealed a 20% decrease(mean±SEM: 104±10.2 vs. 130±10.4 fmol/mg ETE) in the density
of kainate receptors in the CA 2–3 of the ApoD-/- mice. In addition therewas a global decrease inAMPA receptors
(F1,214=4.67, pb0.05) and a global increase in muscarinic M2/M4 receptors (F1,208=22.77, pb0.0001) in the
ApoD-/- mice that did not reach significance in any single cytoarchitectural region. We conclude that
glutamatergic pathways seem to be particularly affected in ApoD-/- mice and this may contribute to the changes
in learning and memory, motor tasks and orientation-based tasks observed in these animals, all of which involve
glutamatergic neurotransmission.
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