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Antiproliferative action of benzodiazepines in cultured brain cells is not mediated through the peripheral-type benzodiazepine acceptor.

Abstract
The benzodiazepines, Ro 5-4864, diazepam, clonazepam, and also PK-11195, inhibited, at micromolar concentrations, the proliferation of rat C6 glioma and mouse neuro-2A neuroblastoma cells in culture. The cells possessed high levels of "peripheral-type" high-affinity benzodiazepine binding sites as judged by binding assays and displacement potencies. However, the different potencies and specificities of compounds for the antiproliferative actions and binding affinities for the binding site suggest that the antiproliferative actions were not mediated through the peripheral-type binding site. In support of this, these compounds have also been shown to inhibit proliferation of some nonneuronal cultured cell lines, e.g., mouse SP2/O-Ag 14 hybridoma and rat NCTC epithelial cells, which have no detectable high-affinity peripheral-type benzodiazepine binding sites.
AuthorsA M Gorman, G B O'Beirne, C M Regan, D C Williams
JournalJournal of neurochemistry (J Neurochem) Vol. 53 Issue 3 Pg. 849-55 (Sep 1989) ISSN: 0022-3042 [Print] England
PMID2547904 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Benzodiazepinones
  • Isoquinolines
  • Receptors, GABA-A
  • Benzodiazepines
  • 4'-chlorodiazepam
  • Clonazepam
  • DNA
  • Diazepam
  • PK 11195
Topics
  • Animals
  • Benzodiazepines (pharmacology)
  • Benzodiazepinones (pharmacology)
  • Blood
  • Cell Division (drug effects)
  • Clonazepam (pharmacology)
  • DNA (biosynthesis)
  • Diazepam (pharmacology)
  • Glioma (metabolism, pathology)
  • Isoquinolines (pharmacology)
  • Mice
  • Neuroblastoma (metabolism, pathology)
  • Rats
  • Receptors, GABA-A (physiology)
  • Tumor Cells, Cultured

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