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Abstract
Maternal infection during pregnancy is a notable risk factor for the offspring to
develop severe neuropsychiatric disorders, including schizophrenia. One prevalent
hypothesis suggests that infection-induced disruption of early prenatal brain development
predisposes the organism for long-lasting structural and functional brain abnormalities,
leading to the emergence of psychopathological behaviour in adulthood. The feasibility
of this causal link has received considerable support from several experimental models
established in both rats and mice. In this review, we provide an integrative summary
of the long-term neuropathological consequences of prenatal exposure to infection
and/or inflammation as identified in various experimental models of prenatal immune
challenge. In addition, we highlight how abnormalities in distinct brain areas and
neurotransmitter systems following prenatal immune activation may provide a neural
basis for the emergence of specific forms of psychosis-related behaviour. Specifically,
we suggest that prenatal infection-induced imbalances in the mesolimibic and mesocortical
dopamine pathways may constitute critical neural mechanisms for disturbances in sensorimotor
gating, abnormalities in selective associative learning and hypersensitivity to psychostimulant
drugs. On the other hand, the emergence of working memory deficiency following prenatal
immune challenge may be crucially linked to the concomitant disruption of GABAergic
and glutamatergic functions in prefrontal cortical and hippocampal structures. Notably,
many of the identified neuronal abnormalities are directly implicated in the neuropathology
of schizophrenia. The findings from prenatal infection models of schizophrenia thus
provide considerable experimental evidence for the assumption that prenatal exposure
to infection and/or inflammation is a relevant environmental link to specific neuronal
abnormalities underlying psychosis-related behaviour in humans.