Delayed Mesolimbic System Alteration in a Developmental Animal Model of Schizophrenia
Abstract
Pharmacological and imaging studies indicate that the prefrontal cortex and nucleus accumbens and their dopamine innervation are central elements of the pathophysiology of schizophrenia. Although symptoms typically appear in young adults, a developmental component has been suggested, primarily in the hippocampus. A neonatal hippocampal lesion in rats and monkeys produces changes resembling schizophrenia symptoms only after the animals reach adulthood, indicating that this procedure could be used as a developmental animal model of this disorder. Here, we explored whether the dopamine projection to the nucleus accumbens becomes functionally altered in these animals. In vivo intracellular recordings revealed abnormal responses in accumbens neurons to activation of their dopamine afferents in adult but not prepubertal animals with a neonatal lesion. This alteration was absent after antipsychotic drug treatment. These results indicate that neonatal hippocampal damage can result in delayed functional deficits in the mesolimbic system, providing a link between the developmental hippocampal deficit and altered dopamine systems postulated to occur in schizophrenia.
Read the paper
Related studies
- A Survey on Knowledge Graphs: Representation, Acquisition, and Applications
- Toxicity of nanomaterials
- The Human Gene Mutation Database: towards a comprehensive repository of inherited mutation data for medical research, genetic diagnosis and next-generation sequencing studies
- Halogen bonding (X‐bonding): A biological perspective
- Biofilm formation at the air–liquid interface by the Pseudomonas fluorescens SBW25 wrinkly spreader requires an acetylated form of cellulose
- Opioid Activation of Toll-Like Receptor 4 Contributes to Drug Reinforcement
Go deeper in Evidence Hub
Evidence Hub adds a study data sheet (design, sample size, evidence level, key numbers), an AI summary and a chat grounded in the paper's text.