No modifications of GABAA and benzodiazepine receptors following experimental dysthyroidism in rats.
The effect of a treatment with L-triiodothyronine (T3) or propylthiouracil (PTU) on the characteristics of benzodiazepine and chloride ion channel binding sites in rat hippocampus and cerebral cortex was studied using a radiolabelled technique. In our experimental conditions, neither hyper- nor hypothyroidism modified number and affinity of [3H]flunitrazepam or [3H]butylbicycloorthobenzoate (TBOB) binding sites. These data indicate that neither benzodiazepine nor chloride ionophore sites of the GABA complex are modified in an experimental condition of dysthyroidism.
Sandrini
M
M
Institute of Pharmacology, University of Modena, Italy.
Vergoni
A V
AV
Bertolini
A
A
D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects; D018118:Chloride Channels / Q000378:metabolism; D004195:Disease Models, Animal; D006624:Hippocampus / Q000187:drug effects; D006980:Hyperthyroidism / Q000139:chemically induced / Q000378:metabolism*; D007037:Hypothyroidism / Q000139:chemically induced / Q000378:metabolism*; D008297:Male; D011441:Propylthiouracil; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000378:metabolism*; D014284:Triiodothyronine; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D018118:Chloride Channels; D011963:Receptors, GABA-A; D014284:Triiodothyronine; D005680:gamma-Aminobutyric Acid; D011441:Propylthiouracil