A Hypothesis of Thyroid-Catecholamine-Receptor Interaction

Myxedema madness complicating postoperative follow-up of thyroid cancer

“…It has been reported that in the limbic system of the rat, hypothyroidism can cause a decrease in serotonin with the consequent up-regulation of dopamine postsynaptic receptors and increased dopamine activity in the brain, resulting in maniac symptoms (12,13). Furthermore, thyroid hormones have a modulating impact on the brain catecholamine system, regulating β-adrenergic receptor sensitivity, so that changes in hormone levels, as seen in hypothyroidism, might increase catecholamine action with major risk of mania in vulnerable individuals (14). Therefore, the influence of an impairment of the thyroid system on neurotransmitters (particularly serotonin and norepinephrine), which play a major role in the regulation of mood and behavior, may contribute to the mechanisms of mood modulation (12,15).…”

Longitudinal evidence of the impact of normal thyroid stimulating hormone variations on cognitive functioning in very old age

“…Importantly, thyroid hormones increase the response of the beta-adrenergic receptor to norepinephrine, which may serve as an adaptive mechanism of neuromodulation (Whybrow and Prange, 1981;Dratman and Gordon, 1996). More specifically, low TSH levels are also associated with elevated steroid hormone levels within the hypothalamus-pituitary-adrenal axis (van Haasteren et al, 1996).…”

The effects of thyroid state on beta-adrenergic and serotonergic receptors in rat brain

“…Clinical depression occurs in about 40% of hypothyroid patients, and in most of these patients replacement therapy produces prompt remission of depressive symptoms (Whybrow et al, 1969Sachar, 1975;Whybrow and Prange, 1981). In depressed patients activation of the thyroid axis, as indicated by increased secretion of thyroid hormones, is predictive of a rapid response to therapy with a tricyclic antidepressant (TCA) (Whybrow and Prange, 1981).…”

“…Clinical depression occurs in about 40% of hypothyroid patients, and in most of these patients replacement therapy produces prompt remission of depressive symptoms (Whybrow et al, 1969Sachar, 1975;Whybrow and Prange, 1981). In depressed patients activation of the thyroid axis, as indicated by increased secretion of thyroid hormones, is predictive of a rapid response to therapy with a tricyclic antidepressant (TCA) (Whybrow and Prange, 1981). Furthermore, concurrent administration of L-triiodothyronine (T 3 ) with a TCA has been found to accelerate the antidepressant effect in women Wilson et al, 1970;Wheatly, 1972;Coppen et al, 1972) and to produce a therapeutic response in patients of both sexes who previously did not respond to TCA treatment alone (Earle;1970;Hatotani et al, 1974;Ogura et al, 1974;Goodwin et al, 1982).…”