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Clozapine increases apolipoprotein d expression in rodent brain: Towards a mechanism for neuroleptic pharmacotherapy

Academic Article
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Overview

authors

  • Thomas, Elizabeth
  • Danielson, P. E.
  • Nelson, P. A.
  • Pribyl, T. M.
  • Hilbush, B. S.
  • Hasel, K. W.
  • Sutcliffe, J. Gregor

publication date

  • February 2001

journal

  • Journal of Neurochemistry  Journal

abstract

  • In contrast to typical neuroleptic drugs, which have high affinities for dopamine D2 receptors, clozapine binds to multiple neurotransmitter receptors. The mechanisms responsible for its superior clinical efficacy over typical neuroleptics remain unknown. Using an automated genomics approach, total gene expression analysis (TOGA), we found an approximately threefold increase in the accumulation of the mRNA encoding apolipoprotein D (apoD) in mouse striatum in response to chronic treatment with clozapine. While in control animals, apoD is expressed predominantly in astrocytes, in situ hybridization and immunohistochemical studies indicated a substantial increase in apoD expression in neurons of the striatum, globus pallidus and thalamus after 2 weeks of clozapine treatment. Clozapine-induced increases in apoD expression were also observed in some white matter regions. These results suggest that apoD is a mediator in the mechanisms of clozapine and thus that deficiencies in aspects of lipid metabolism may be responsible for psychoses.

subject areas

  • Animals
  • Antipsychotic Agents
  • Apolipoproteins
  • Apolipoproteins D
  • Brain
  • Clozapine
  • Male
  • Mice
  • Mice, Inbred C57BL
  • RNA, Messenger
  • Reference Values
  • Time Factors
  • Tissue Distribution
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Research

keywords

  • astrocyte
  • glia
  • in situ hybridization
  • lipid
  • neuropathology
  • psychoses
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Identity

International Standard Serial Number (ISSN)

  • 0022-3042

Digital Object Identifier (DOI)

  • 10.1046/j.1471-4159.2001.00027.x

PubMed ID

  • 11158250
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Additional Document Info

start page

  • 789

end page

  • 796

volume

  • 76

issue

  • 3

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