<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Meyer U</dc:creator>
  <dc:creator>Feldon J</dc:creator>
  <dc:date>2012</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">The neurodevelopmental hypothesis of schizophrenia has been highly influential in shaping our current thinking about modeling the disease in animals. Based on the findings provided by human epidemiological studies, a great deal of recent interest has been centered upon the establishment of neurodevelopmental rodent models in which the basic experimental manipulation takes the form of prenatal exposure to infection and/or immune activation. One such model is based on prenatal treatment with the inflammatory agent poly(I:C) (=polyriboinosinic-polyribocytidilic acid), a synthetic analog of double-stranded RNA. Since its initial establishment and application to basic schizophrenia research, the poly(I:C) model has made a great impact on researchers concentrating on the neurodevelopmental and neuroimmunological basis of complex human brain disorders such as schizophrenia, and as a consequence, the model now enjoys wide recognition in the international scientific community. The present article emphasizes that the poly(I:C) model has gained such impact because it successfully accounts for several aspects of schizophrenia epidemiology, pathophysiology, symptomatology, and treatment. The numerous features of this experimental system make the poly(I:C) model a very powerful neurodevelopmental animal model of schizophrenia-relevant brain disease which is expected to be capable of critically advancing our knowledge of how the brain, following an (immune-associated) triggering event in early life, can develop into a "schizophrenia-like brain" over time. Furthermore, the poly(I:C) model seems highly suitable for the exploration of novel pharmacological and neuro-immunomodulatory strategies for both symptomatic and preventive treatments against psychotic disease, as well as for the identification of neurobiological mechanisms underlying gene-environment and environment-environment interactions presumably involved in the etiology of schizophrenia and related disorders.</dc:description>
  <dc:identifier>https://sonar.ch/global/documents/36444</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1016/j.neuropharm.2011.01.009</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/21238465</dc:relation>
  <dc:source>Neuropharmacology. - 2012</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Animals</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Disease Models, Animal</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Female</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Humans</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Neuroimmunomodulation</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Poly I-C</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Pregnancy</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Prenatal Exposure Delayed Effects</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Schizophrenia</dc:subject>
  <dc:title xmlns:ns10="xml" ns10:lang="en">To poly(I:C) or not to poly(I:C): advancing preclinical schizophrenia research through the use of prenatal immune activation models.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>