Abstract
The study was aimed at investigating the repercussions of deficiency in thyroid function with and without thyroid hormone (TH) replacement on the neurochemical entities which underly serotonin (5-HT) neutrotransmission, namely 5-HT<sub>1A</sub>, 5-HT<sub>2A</sub> receptors, 5-HT transporter and tryptophan hydroxylase (TPH) in the mature brain. Surgically thyroidectomized male Wistar rats received: (1) an iodine-free diet to produce severe hypothyroidism; (2) hormonal replacement with 15 µg/kg/day of thyroxine (T4) for 21 days to normalize serum TH levels, or (3) hormonal replacement with 200 µg/kg/day of T4 for 14 days to produce an excess of circulating THs. Sham-operated rats were used as controls. Neither hypothyroidism nor an excess in serum TH levels affected <sup>3</sup>H-8-OH-DPAT binding to 5-HT<sub>1A</sub> receptors, <sup>3</sup>H-citalopram binding to 5-HT transporter and TPH activity in various brain structures indicating that, in the mature brain, the presynaptic entities of 5-HT neurotransmission are resistant to large variations in TH levels. By contrast, hypothyroid rats had a significant decrease in B<sub>max</sub> of <sup>3</sup>H-ketanserin binding to cortical 5-HT<sub>2A</sub> receptors compared to controls. Cortical <sup>3</sup>H-ketanserin binding in thyroidectomized rats was normalized after replacement with low-dose T4. Excess serum TH levels in thyroidectomized rats did not produce any changes in cortical 5-HT<sub>2A</sub> receptors when compared to thyroidectomized rats with normalized TH levels. The present data suggest that the decrease in cortical 5-HT<sub>2A</sub> receptors is the main neurochemical event underlying the impairing effect of hypothyroidism on 5-HT neurotransmission.
Published Version
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