Abstract
Clinical studies consistently report structural impairments (i.e.: ventricular enlargement, decreased volume of anterior cingulate cortex or hippocampus) and functional abnormalities including changes in regional cerebral blood flow in individuals suffering from schizophrenia, which can be evaluated by magnetic resonance imaging (MRI) techniques. The aim of this study was to assess cerebral blood perfusion in several schizophrenia-related brain regions using Arterial Spin Labelling MRI (ASL MRI, 9.4 T Bruker BioSpec 94/30USR scanner) in rats. In this study, prenatal exposure to methylazoxymethanol acetate (MAM, 22 mg/kg) at gestational day (GD) 17 and the perinatal treatment with Δ-9-tetrahydrocannabinol (THC, 5 mg/kg) from GD15 to postnatal day 9 elicited behavioral deficits consistent with schizophrenia-like phenotype, which is in agreement with the neurodevelopmental hypothesis of schizophrenia. In MAM exposed rats a significant enlargement of lateral ventricles and perfusion changes (i.e.: increased blood perfusion in the circle of Willis and sensorimotor cortex and decreased perfusion in hippocampus) were detected. On the other hand, the THC perinatally exposed rats did not show differences in the cerebral blood perfusion in any region of interest. These results suggest that although both pre/perinatal insults showed some of the schizophrenia-like deficits, these are not strictly related to distinct hemodynamic features.
Highlights
Schizophrenia (SCZ) is a debilitating mental illness condition affecting both brain structure and function[1]
MAM rats exhibited a cognitive deficit in the Novel object recognition test (NORT) measured by decreased discrimination index (MWU test, p = 0.022)
Pre/perinatal insults by MAM and THC led to behavioral impairments observed in this study, which are consistent with several neuropsychiatric disorders including SCZ, they were not characterized by the same regional cerebral blood flow (CBF) alterations
Summary
Schizophrenia (SCZ) is a debilitating mental illness condition affecting both brain structure and function[1]. A meta-analysis of clinical studies confirmed consistently reported progressive ventricular (lateral and third) enlargement, along with decreased volume of amygdala, anterior cingulate cortex, frontal and temporal lobes, hippocampus and thalamus[2] These changes are paralleled by functional abnormalities detected by neuroimaging methods. A meta-analysis of functional neuroimaging studies employing nuclear medicine imaging techniques (PET, SPECT) or blood-oxygen level determination MRI reported reduced activation in the insula/superior temporal gyrus and the medial frontal/anterior cingulate cortex in SCZ suffering patients. These changes were partly worsened by antipsychotic treatment[1]. We have further assessed two other brain regions highly relevant for SCZ – the anterior cingulate cortex which is part of the prefrontal cortex[1,20,21] and the striatum, i.e. the caudate putamen[2,22,23]
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