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Pharmacological and proteomic analyses of neonatal polyI:C-treated adult mice

Kanako Kitagawa1, Taku Nagai1, Kiyofumi Yamada1

  • 1Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Nagoya 466-8560, Japan.

Neuroscience Research
|August 27, 2019
PubMed

Insights

Neonatal viral infection models, like polyI:C exposure in mice, show promise for studying neurodevelopmental disorders. Antipsychotics like clozapine demonstrate potential in ameliorating associated behavioral deficits.

Area of Science:

  • Neuroscience
  • Immunology
  • Pharmacology

Background:

  • Perinatal viral infections are linked to neurodevelopmental disorders, including schizophrenia.
  • Neonatal exposure to polyriboinosinic-polyribocytidilic acid (polyI:C), a viral mimetic, induces adolescent behavioral and cognitive deficits in mice.
  • Understanding the impact of immune activation on brain development is crucial for identifying therapeutic targets.

Purpose of the Study:

  • To investigate the efficacy of antipsychotic medications in ameliorating polyI:C-induced behavioral abnormalities in a mouse model.
  • To identify molecular changes in the hippocampus associated with neonatal immune activation using proteomic analysis.
  • To explore the potential of this model for evaluating novel antipsychotic compounds.

Main Methods:

  • Neonatal mice received daily subcutaneous injections of polyI:C from postnatal day 2 to 6.
  • At 10 weeks of age, behavioral tests assessed sensorimotor gating, emotional regulation, and cognitive function.
  • Hippocampal proteomic analysis was performed using two-dimensional electrophoresis on polyI:C-treated adult mice.

Main Results:

  • Clozapine treatment improved prepulse inhibition (PPI) deficits, as well as emotional and cognitive dysfunctions in polyI:C-exposed mice.
  • Haloperidol treatment solely improved the PPI deficit in the polyI:C model.
  • Proteomic analysis identified aldehyde dehydrogenase family 1 member L1 (ALDH1L1) and collapsin response mediator protein 5 (CRMP5) as differentially expressed proteins in the hippocampus.

Conclusions:

  • The polyI:C mouse model is a valuable tool for assessing the antipsychotic potential of therapeutic agents.
  • Altered expression of ALDH1L1 and CRMP5 suggests a role for astrocyte-neuron interactions in the neurodevelopmental consequences of neonatal immune activation.
  • These findings contribute to understanding the pathophysiology of neurodevelopmental disorders triggered by early-life immune challenges.

Keywords:
Animal modelAntipsychotic drugsBehaviorProteomicsSchizophreniaViral infectionpolyI:C

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