“In Vivo” Inhibition of GABAergic Transmission Increases 35S-TBPS Binding in the Rat Brain

  • G. Biggio
  • E. Sanna
  • M. Serra
  • G. P. Serra
  • A. Concas
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 287)


Several lines of evidence have well established that the cage convulsant t-butylbicyclophosphorothionate (TBPS) inhibits the function of the central GABAergic transmission by binding to specific recognition sites present at the level of the chloride ionophore coupled to the GABAA/benzodiazepine receptor complex (Squires et al., 1983; Van Renterghem et al., 1987). This finding has given a rather unique tool to study biochemically the function of the GABA-dependent chloride channel. In fact, the specific binding of 35S-TBPS to the recognition sites associated to the GABAA receptor complex is modulated in an opposite manner by different compounds which specifically enhance (GABA agonists, benzodiazepines, imidazopyridines, anxiolytic and anticonvulsant ß-carbolines etc.) and inhibit (GABA antagonists, anxiogenic and convulsant ß-carbolines etc.) the function of the GABA-dependent chloride channel, respectively (Squires et al., 1983; Gee et al., 1986; Concas et al., 1988; Biggio et al., 1989; Serra et al., 1989; Sanna et al., 1990).


Valproic Acid Chloride Channel Kainic Acid GABAergic Transmission Gaba Content 
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Copyright information

© Plenum Press, New York 1991

Authors and Affiliations

  • G. Biggio
    • 1
  • E. Sanna
    • 1
  • M. Serra
    • 1
  • G. P. Serra
    • 1
    • 2
  • A. Concas
    • 1
  1. 1.Department of Experimental Biology, Chair of PharmacologyUniversity of CagliariItaly
  2. 2.Institute of ZoologyUniversity of CagliariItaly

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