Abstract:
:Vervet monkeys were pharmacologically treated acutely and with repeated dose loading to alter serotonergic systems to assess the role of serotonin in the regulation of the hypothalamus-pituitary-thyroid axis. Acute L-tryptophan administration failed to alter basal levels of thyroid hormones but did decrease the TRH-induced TSH response. Repeated dose loading of tryptophan or 5-hydroxytryptophan increased blood serotonin and plasma T3 and decreased plasma TSH. The tryptophan hydroxylase inhibitor p-chlorophenylalanine yielded decreased blood serotonin, but did not affect plasma TSH, T4 or T3. The monoamine oxidase inhibitor chlorgyline also resulted in increased blood serotonin, but increased plasma TSH and T4 and decreased T3. These data may be explained by a unitary hypothesis involving central catecholaminergic, rather than serotonergic, control of TRH release. Chlorgyline may produce its effects predominantly by facilitating catecholaminergic stimulation of TRH release resulting in increased TSH and a consequent increase in T4. It is suggested that the effects of tryptophan and 5-hydroxytryptophan result from increases in serotonin levels in the thyroid gland to produce an increase in T3 with a compensatory decrease in TSH via negative feedback. The differences observed between the acute and repeated dose loading studies stress the need for both types of studies before drawing conclusions about the effects of pharmacological manipulations on hormonal levels.
journal_name
Eur J Pharmacoljournal_title
European journal of pharmacologyauthors
Morley JE,Raleigh MJ,Brammer GL,Yuwiler A,Geller E,Flannery J,Hershman JMdoi
10.1016/0014-2999(80)90509-9subject
Has Abstractpub_date
1980-10-17 00:00:00pages
283-8issue
2-3eissn
0014-2999issn
1879-0712pii
0014-2999(80)90509-9journal_volume
67pub_type
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