Thyroid Activity Following Intracerebral Injection of Morphine in the Rat

The effects of morphine (10 mg i.v.), an opioid agonist, and of naloxone (10 mg i.v.), an opioid antagonist, on serum levels of TSH and PRL were studied in 7 hypothyroid patients and in 5 normal volunteers. Morphine administration induced a prompt, significant increase in serum TSH and PRL in all subjects. The degree of PRL release after morphine was similar in the two groups, while, as regards TSH, the increase was more evident in hypothyroid subjects. Pretreatment with naloxone (4 mg i.v. 5 min before morphine administration) blocked these effects in all subjects. In contrast, naloxone alone was not able to affect significantly TSH and PRL secretion. Moreover, in 5 other euthyroid volunteers, morphine significantly enhanced the response of TSH and PRL to TRH stimulation (200 µg i.v.).

Section: Discussionmentioning

confidence: 99%

Morphine-Induced TSH Release in Normal and Hypothyroid Subjects

Devilla¹,

Pende²,

Morgano³

et al. 1985

“…The influence of opioid peptides on TSH secretion is well documented in animals: the acute administration of morphine or Met-enkephalin to rats in vivo depressed TSH release and thyroid function [3,19], while the concurrent injection of naloxone partially counteracted this effect [3,22]. In vitro May et al [21] de monstrated a TSH release-inhibiting activity by Leu-enkephalin on rat hemipituitaries.…”

Section: Discussionmentioning

confidence: 99%

Naloxone and Anterior Pituitary Hormones: Effect on TRH Stimulation Test

Zanoboni¹,

Zecca²,

Zanussi³

et al. 1981

A specific opiate antagonist, naloxone, administered i.v. to 5 normal men at the doses of 0.4 mg or 0.8 mg in bolus, did not modify basal PRL, GH, TSH and FSH levels, but significantly increased basal LH concentrations at the dose of 0.8 mg. Naloxone at both doses was also able to significantly enhance the response of TSH to a TRH stimulation test (TRH 400 μg i.v. in bolus) but did not alter significantly the PRL response. These results suggest that endogenous opioid peptides may have an influence on the modulation of LH secretion in basal conditions and on the responsiveness of TSH to dynamic stimulation by TRH.

“…There are several reports that in rats, morphine [10, 63,76,87,116] or metenkephalin [10] lowered basal serum TSH levels or inhibited activation of TSH secretion by cold or thyroidectomy [87, I 16]. Mor phine did not, however, inhibit the TRH-stimulated TSH surge and according to one group of investigators [87] it ac tually potentiated the effect of TRH.…”

Section: Other Transmittersmentioning

confidence: 99%

Neurotransmitter Control of Thyrotropin Secretion

Krulich

1982

The central dopaminergic system seems to have an inhibitory influence on the secretion of thyrotropin (TSH) both in humans and rats. This is documented by observations that in humans, especially in subjects with primary hypothy-roidism, the dopamine precursor l-Dopa, dopamine receptor agonist bromocryptine, and dopamine itself decrease plasma levels of TSH and in some instances inhibit TSH secretory response to thyrotropin-releasing hormone (TRH). Conversely blockade of dopamine receptors leads to an elevation of circulating TSH. It is probable the dopaminergic drugs act on the pituitary thyrotrops rather than on the release of hypothalamic TRH. Analogous results were obtained in rats. In contrast, the noradrenergic system, studied mainly in rats, has a stimulatory influence on the secretion of TSH. This view is mainly supported by findings that acute interruption of noradrenergic neurotransmission causes a decrease of serum TSH levels and blocks the cold-induced stimulation of TSH secretion. The role of the central serotonergic system remains undecided because some experimental findings indicate that it has an inhibitory influence but others indicate an opposite function. The remaining transmitter systems have not been studied extensively enough to allow definite conclusions about their roles in the regulation of TSH secretion.