Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P08908 (5-HT1A)
 5,574 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of dysthyroidism on central 5-HT1A receptor subtype in adult Wistar rats were investigated. Hyperthyroidism and hypothyroidism were respectively produced with the administration of T3 and propylthiouracil (PTU) via gavage for 2 weeks. Heart rate, oxygen consumption, anal temperature and plasma T3 concentration were increased in hyperthyroid rats and decreased in hypothyroid rats significantly. Radioligand binding assay showed that the specific binding of [3H] 8-hydroxy-2-(di-n-propylamino) tetralin ([3H] 8-OH-DPAT) at 0.6 nmol/L concentration was highest in hippocampus, next in cerebral cortex, and lowest in hypothalamus, brain stem and corpus striatum in euthyroid rats. Hyperthyroidism increased the binding significantly in hippocampus but decreased in cortex. No change was found in the other brain regions. Scatchard analyses revealed that the Bmax was increased in hippocampus and decreased in cortex, whereas the KD was not consistently affected in hyperthyroid rats in comparison with that in euthyroid rats. However, there were no significant changes mentioned above in all these brain regions of hypothyroid rats. Our results indicate that there seems to exist an imbalance of the serotonergic activity mediated via 5-HT1A receptor between hippocampus and cerebral cortex in hyperthyroids. This might be one of the mechanisms leading to psychoneural disorders in hyperthyroidism.
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PMID:[Effects of different thyroid states on 5-HT1A receptor in adult rat brain]. 159 97

Pharmacology can contribute in four ways to our understanding and to the management of resistant depression: 1) Dosage: some antidepressants have an inverted-U dose-response curve, i.e. the response disappears when dosage is increased. In man, dose-response relationships are not well established because the curves are obtained with groups of patients and they reflect an overall mean rather than the reality of each individual patient. 2) Secondary regulatory adaptive mechanism such as: down regulation of beta, 5-HT2, alpha-2 receptors--increased reactivity of 5-HT1A, alpha-1 and dopaminergic systems. Defective development of these mechanisms is thought to originate resistance in certain cases, which could therefore be corrected more or less specifically by adding thyroid hormone, lithium, an alpha-2 agonist or even by switching to a 5-HT1A agonist or a dopaminergic drug. 3) Biological resistance factors: it has been shown in the rat that hypothyroidism, diabetes, weight loss cause a decrease in beta-adrenergic system reactivity, and therefore a resistance to noradrenergic antidepressants. 4) Co-prescription: the efficacy of noradrenergic antidepressants is known to involve the activation of beta-adrenergic receptors. Animal studies have shown that the co-prescription of a beta-blocker nullifies this efficacy. Benzodiazepines decrease serotonergic and noradrenergic neuronal activity: animal studies have shown that they antagonize most antidepressants. What happens in depressed humans who are often co-prescribed these drugs? I would like to share with you a few data from experimental pharmacology which may help us to think differently, not when faced to a patient with resistant depression, but when confronted with the failure of a well conducted antidepressant treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Contributions of pharmacology in the treatment of resistance to antidepressive agents]. 828 6

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-HT1A, 5-HT2A 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 microgram/kg/day of thyroxine (T4) for 21 days to normalize serum TH levels, or (3) hormonal replacement with 200 microgram/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 3H-8-OH-DPAT binding to 5-HT1A receptors, 3H-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 Bmax of 3H-ketanserin binding to cortical 5-HT2A receptors compared to controls. Cortical 3H-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-HT2A receptors when compared to thyroidectomized rats with normalized TH levels. The present data suggest that the decrease in cortical 5-HT2A receptors is the main neurochemical event underlying the impairing effect of hypothyroidism on 5-HT neurotransmission.
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PMID:Effects of experimental hypothyroidism on 5-HT1A, 5-HT2A receptors, 5-HT uptake sites and tryptophan hydroxylase activity in mature rat brain1. 1036 98

Effects of thyroid hormone deficiency on 5-HT1A receptors, 5-HT2A receptors and serotonin transporter in the brain were studied in thyroidectomised Wistar rats receiving an iodine-free diet and receiving 15 micrograms/kg of thyroxine for 21 days. Binding of 3H-8-OH-DPAT to 5-HT1A receptors and 3H-cytalopram to serotonin transporter were unchanged in hypothyroid rats as compared to the control. 3H-ketanserin binding to 5-HT2A receptors was significantly decreased in the frontal cortex in hypothyroid rats. The cortical 3H-ketanserin binding in thyroidectomised rats was normalised after thyroxine replacement. The data suggest that the decrease in the cortical 5-HT2A receptors is the main consequence of impairing effect of hypothyroidism on serotonin neurotransmission.
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PMID:[Effect of hypothyroidism on 5-HT1A-, 5-HT2A-receptors and serotonin transporter in the rat brain]. 1080 28