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Benzodiazepine Receptor and Thyroid Hormones: In Vivo and In Vitro Modulation
Author(s) -
Medina Rjorge H.,
Robertis Eduardo
Publication year - 1985
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1985.tb08767.x
Subject(s) - in vivo , hormone , in vitro , modulation (music) , thyroid , thyroid hormones , thyroid hormone receptor , receptor , endocrinology , gabaa receptor , medicine , chemistry , neuroscience , biology , biochemistry , physics , microbiology and biotechnology , acoustics
In rats rendered hyperthyroid by chronic treatment with L‐triiodothyronine (T 3 ) hormone there was a 21 and 27% decrease, respectively, in the number of binding sites for [ 3 H]flunitrazepam ([ 3 H]FNZ) and [ 3 H]ethyl‐β‐carboline‐3‐carboxylate ([ 3 H]β‐CCE) without changes in affinity for the two ligands. Two weeks after thyroidectomy there was a 44% increase in [ 3 H]FNZ sites and a 17% increase in [ 3 H]β‐CCE binding sites. In vitro we found that T 3 produces a decrease in B max and an increase in K D , both changes being characteristic of a mixed type of inhibition. Thyroid status dramatically affected the K i of T 3 in displacing [ 3 H]FNZ from sites on isolated membranes of the cerebral cortex: in hypothyroid rats the K i value was 0.9 μ M , whereas in hyperthyroid rats it was 83 μ M , a 92‐fold difference. In control rats, the K i was 11 μ M These findings are discussed in relation to a possible modulation of benzodiazepine receptors by thyroid hormones.