Central effects of tricyclic compounds on the endocrine system - An in vitro study

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Abstract

The present study involves the effects on corticotropin (ACTH) release of neuro- and thymoleptic tricyclic antidepressant compounds (TrcACs: chlorpromazine, promethazine, haloperidol, imipramine, amitriptyline) and their interactions with lysine-8-vasopressin (LVP) and corticosterone (B). As an in vitro model, 14-day monolayer pituitary cell cultures of Wistar rats were employed. The ACTH concentrations of the supernatant media were measured by radioimmunoassay. TrcACs augmented ACTH release; their combination with LVP, however, did not result in further stimulation; moreover, when combined with TrcACs + LVP, B did not inhibit, but rather paradoxically increased their ACTH-releasing action. As none of these phenomena were followed by relevant changes in intracellular cyclic adenosine monophosphate content, the mechanism of action may be proposed to involve a protein kinase C route.

Original languageEnglish
Pages (from-to)89-92
Number of pages4
JournalProgress in Brain Research
Volume91
Publication statusPublished - 1992

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Endocrine System
Adrenocorticotropic Hormone
Lypressin
Promethazine
Amitriptyline
Imipramine
Tricyclic Antidepressive Agents
Chlorpromazine
Haloperidol
Corticosterone
Cyclic AMP
Protein Kinase C
Antidepressive Agents
Radioimmunoassay
Wistar Rats
Cell Culture Techniques
In Vitro Techniques

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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abstract = "The present study involves the effects on corticotropin (ACTH) release of neuro- and thymoleptic tricyclic antidepressant compounds (TrcACs: chlorpromazine, promethazine, haloperidol, imipramine, amitriptyline) and their interactions with lysine-8-vasopressin (LVP) and corticosterone (B). As an in vitro model, 14-day monolayer pituitary cell cultures of Wistar rats were employed. The ACTH concentrations of the supernatant media were measured by radioimmunoassay. TrcACs augmented ACTH release; their combination with LVP, however, did not result in further stimulation; moreover, when combined with TrcACs + LVP, B did not inhibit, but rather paradoxically increased their ACTH-releasing action. As none of these phenomena were followed by relevant changes in intracellular cyclic adenosine monophosphate content, the mechanism of action may be proposed to involve a protein kinase C route.",
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