Author Correction: Behavioral abnormalities with disruption of brain structure in mice overexpressing VGF.

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Sensorimotor gating deficits and effects of antipsychotics on the hyperactivity in VGF-overexpressing mice.

BACKGROUND: VGF nerve growth factor inducible (VGF) is a neuropeptide which is expressed in neuronal cells and endocrine cells. VGF is induced by several neurotrophic factors. The expression level of VGF in patients with schizophrenia is increased in cerebrospinal fluid (CSF) and prefrontal cortex. In our previous study, we generated mice in which the expression level of VGF in the brain was increased. VGF-overexpressing mice exhibited abnormal behaviors including hyperactivity. However, it remains unknown whether VGF-overexpressing mice exhibit the endophenotype of schizophrenia and whether abnormal behaviors in these mice can be improved by antipsychotics. METHODS: In the present study, we investigated schizophrenia-like behaviors and the responsiveness to antipsychotics in transgenic mice. RESULTS: VGF-overexpressing mice (1) exhibited prepulse inhibition (PPI) impairment, (2) showed normalized hyperactivity following antipsychotic drug treatment, and (3) showed abnormal responsiveness to haloperidol. CONCLUSION: Upregulation of VGF may be implicated in the pathophysiology of schizophrenia and abnormalities of dopaminergic signaling.

Behavioral abnormalities with disruption of brain structure in mice overexpressing VGF.

VGF nerve growth factor inducible (VGF) is a neuropeptide induced by nerve growth factor and brain-derived neurotrophic factor. This peptide is involved in synaptic plasticity, neurogenesis, and neurite growth in the brain. Patients with depression and bipolar disorder have lower-than-normal levels of VGF, whereas patients with schizophrenia and other cohorts of patients with depression have higher-than-normal levels. VGF knockout mice display behavioral abnormalities such as higher depressive behavior and memory dysfunction. However, it is unclear whether upregulation of VGF affects brain function. In the present study, we generated mice that overexpress VGF and investigated several behavioral phenotypes and the brain structure. These adult VGF-overexpressing mice showed (a) hyperactivity, working memory impairment, a higher depressive state, and lower sociality compared with wild-type mice; (b) lower brain weight without a change in body weight; (c) increased lateral ventricle volume compared with wild-type mice; and (d) striatal morphological defects. These results suggest that VGF may modulate a variety of behaviors and brain development. This transgenic mouse line may provide a useful model for research on mental illnesses.