ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012
Early prefrontal functional blockade in rats results in schizophrenia-related anomalies in behavior and dopamine.
Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 15 citations in OpenAlex.
- Tyrosine phosphorylation of the transmembrane protein SIRPα: Sensing synaptic activity and regulating ectodomain cleavage for synapse maturation.The Journal of biological chemistry · 2018Article
- Regional brain dysregulation of Ca(2+)-handling systems in ketamine-induced rat model of experimental psychosis.Cell and tissue research · 2016Article
- Abnormalities in white matter microstructure associated with chronic ketamine use.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Consequences at adulthood of transient inactivation of the parahippocampal and prefrontal regions during early development: new insights from a disconnection animal model for schizophrenia.Frontiers in behavioral neuroscience · 2014Review
- Functional imaging of cortical feedback projections to the olfactory bulb.Frontiers in neural circuits · 2014Article
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Authors and funding
2 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Growing evidence suggests schizophrenia may arise from abnormalities in early brain development. The prefrontal cortex (PFC) stands out as one of the main regions affected in schizophrenia. Latent inhibition, an interesting cognitive marker for schizophrenia, has been found in some studies to be reduced in acute patients. It is generally widely accepted that there is a dopaminergic dysfunctioning in schizophrenia. Moreover, several authors have reported that the psychostimulant, D-amphetamine (D-AMP), exacerbates symptoms in patients with schizophrenia. We explored in rats the effects in adulthood of neonatal transient inactivation of the PFC on behavioral and neurochemical anomalies associated with schizophrenia. Following tetrodotoxin (TTX) inactivation of the left PFC at postnatal day 8, latent inhibition-related dopaminergic responses and dopaminergic reactivity to D-AMP were monitored using in vivo voltammetry in the left core part of the nucleus accumbens in adult freely moving rats. Dopaminergic responses and behavioral responses were followed in parallel. Prefrontal neonatal inactivation resulted in disrupted behavioral responses of latent inhibition and latent inhibition-related dopaminergic responses in the core subregion. After D-AMP challenge, the highest dose (1.5 mg/kg i.p.) induced a greater dopamine increase in the core in rats microinjected with TTX, and a parallel increase in locomotor activity, suggesting that following prefrontal neonatal TTX inactivation animals display a greater behavioral and dopaminergic reactivity to D-AMP. Transitory inactivation of the PFC early in the postnatal developmental period leads to behavioral and neurochemical changes in adulthood that are meaningful for schizophrenia modeling. The data obtained may help our understanding of the pathophysiology of this disabling disorder.
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