Post-weaning social isolation-rearing of rats leads to behavioural and neurochemical sequelae that model aspects of
schizophrenia, and it may be useful to test hypotheses related to putative molecular mechanisms of the illness. In humans, the presynaptic
protein CDCrel-1 represents an interesting candidate molecule for the mechanism and aetiology of
schizophrenia. CDCrel-1 modulates
dopamine neurotransmission, binds to the
SNARE protein syntaxin and maps onto a region of chromosome 22q11 deleted in velo-cardio-facial and DiGeorge syndromes, which are associated with increased prevalence of
schizophrenia. Using the isolation-rearing model, we measured immunoreactivity of the synaptic
proteins CDCrel-1,
synaptophysin and
syntaxin. Male, Sprague-Dawley rats were raised in groups or in isolation for 12 weeks from weaning. Synaptic
protein immunoreactivities were measured in striatal and hippocampal homogenates, using a sensitive
enzyme-linked
immunoadsorbent assay with
monoclonal antibodies. Isolation-rearing produced region- and
protein-specific effects. CDCrel-1 immunoreactivity was significantly lower in the striatum and marginally higher in the hippocampus of isolation-reared compared with socially reared animals. There were no statistically significant differences in
synaptophysin immunoreactivity in either region. Confocal microscopy demonstrated a high degree of colocalization between the two presynaptic
proteins. In striatum, a robust relationship between CDCrel-1 and
syntaxin immunoreactivities was observed in socially reared rats, this was lost in the isolation-reared animals. Altered levels of the
septin CDCrel-1 in isolation-reared rats may contribute to changes in neuronal connectivity and neurotransmission, and suggest a potential role for CDCrel-1 in
schizophrenia related to chromosome
22q11 deletion syndrome.