1974
DOI: 10.1016/0028-3908(74)90063-x
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The effect of tri-iodothyronine in combination with imipramine on [3H]-cyclic AMP production in slices of rat cerebral cortex

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Cited by 92 publications
(16 citation statements)
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“…Although the major emphasis of the work of Schmidt and Schultz ( 1985) is on cortical cyclic AMP generating systems, and not the beta-adrenoceptor per se, their finding that T, or T 4 down-regulates cortical beta-receptors in some strains of rats seems discordant with the present report and that of Perumal et al (1984), as well as with earlier studies by Frazer et al (1974) and Gross et al (1980b) on the effects of thyroid status on the cortical adenylate cyclase system. Nevertheless, in the light of theories that advocate down-regulation ofbeta-adrenergic receptorcoupled adenylate cyclase systems as the mechanism of action of antidepressant drugs, their findings are consistent with the clinical observation that small doses of thyroid hormones can potentiate the action of antidepressant drugs.…”
Section: Discussionsupporting
confidence: 66%
“…Although the major emphasis of the work of Schmidt and Schultz ( 1985) is on cortical cyclic AMP generating systems, and not the beta-adrenoceptor per se, their finding that T, or T 4 down-regulates cortical beta-receptors in some strains of rats seems discordant with the present report and that of Perumal et al (1984), as well as with earlier studies by Frazer et al (1974) and Gross et al (1980b) on the effects of thyroid status on the cortical adenylate cyclase system. Nevertheless, in the light of theories that advocate down-regulation ofbeta-adrenergic receptorcoupled adenylate cyclase systems as the mechanism of action of antidepressant drugs, their findings are consistent with the clinical observation that small doses of thyroid hormones can potentiate the action of antidepressant drugs.…”
Section: Discussionsupporting
confidence: 66%
“…12,16,17 We have found that those antidepressants that cause this effect do so most robustly in certain amygdaloidal nuclei, such as its basolateral nucleus. 18 Moreover, down-regulation of ␤ 1 adrenoceptors is only produced by drugs that acutely enhance noradrenergic function; SSRIs, for example, do not produce this effect ( Figure 2).…”
Section: Delayed Pharmacological Effects Of Antidepressantsmentioning
confidence: 99%
“…Down-regulation of J3-adrenergic receptors after long-term administration of tricyclic antidepressant drugs (Frazer et al 1974;Banerjee et al 1977) and elec troconvulsive shock (Bergstrom and Kellar, 1977) may depend not only on the input from NE neurons (Wolfe et al 1978), but also on 5-HT innervation (Brunello et al 1982;Janowsky et al 1982). Since selective lesions 5-HT and NE Uptake Inhibitor 31 of 5-HT terminals with 5,7-dihydroxytryptamine, but not merely inhibition of 5-HT synthesis by p-chloro phenylalanine, prevent down-regulation of J3-adren ergic receptors by antidepressant treatments, a factor present in 5-HT terminals other than 5-HT itself may be involved (Nimgaonkar et al 1985).…”
Section: Food Intake Studiesmentioning
confidence: 99%