ScholarWorksIndianapolis
  • Communities & Collections
  • Browse ScholarWorks
  • English
  • Català
  • Čeština
  • Deutsch
  • Español
  • Français
  • Gàidhlig
  • Italiano
  • Latviešu
  • Magyar
  • Nederlands
  • Polski
  • Português
  • Português do Brasil
  • Suomi
  • Svenska
  • Türkçe
  • Tiếng Việt
  • Қазақ
  • বাংলা
  • हिंदी
  • Ελληνικά
  • Yкраї́нська
  • Log In
    or
    New user? Click here to register.Have you forgotten your password?
  1. Home
  2. Browse by Author

Browsing by Author "DUNCAN, GARY E."

Now showing 1 - 1 of 1
Results Per Page
Sort Options
  • Loading...
    Thumbnail Image
    Item
    Antipsychotic drugs: comparison in animal models of efficacy, neurotransmitter regulation, and neuroprotection
    (American Society for Pharmacology & Experimental Therapeutics, 2008-09) LIEBERMAN, JEFFREY A.; BYMASTER, FRANK P.; MELTZER, HERBERT Y.; DEUTCH, ARIEL Y.; DUNCAN, GARY E.; MARX, CHRISTINE E.; APRILLE, JUNE R.; DWYER, DONARD S.; LI, XIN-MIN; MAHADIK, SAHEBARAO P.; DUMAN, RONALD S.; PORTER, JOSEPH H.; MODICA-NAPOLITANO, JOSEPHINE S.; NEWTON, SAMUEL S.; CSERNANSKY, JOHN G.; Department of Psychiatry, IU School of Medicine
    Various lines of evidence indicate the presence of progressive pathophysiological processes occurring within the brains of patients with schizophrenia. By modulating chemical neurotransmission, antipsychotic drugs may influence a variety of functions regulating neuronal resilience and viability and have the potential for neuroprotection. This article reviews the current literature describing preclinical and clinical studies that evaluate the efficacy of antipsychotic drugs, their mechanism of action and the potential of first- and second-generation antipsychotic drugs to exert effects on cellular processes that may be neuroprotective in schizophrenia. The evidence to date suggests that although all antipsychotic drugs have the ability to reduce psychotic symptoms via D(2) receptor antagonism, some antipsychotics may differ in other pharmacological properties and their capacities to mitigate and possibly reverse cellular processes that may underlie the pathophysiology of schizophrenia.
About IU Indianapolis ScholarWorks
  • Accessibility
  • Privacy Notice
  • Copyright © 2025 The Trustees of Indiana University