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Effect of 5-hydroxytryptophan on prolactin and growth hormone release in the infant rat: evidence for different
Insights
In infant rats, 5-hydroxytryptophan (5-HTP) increases prolactin (Prl) via serotonin (5-HT) pathways. Growth hormone (GH) release is modulated by catecholaminergic systems, not directly by 5-HT.
Area of Science:
- Neuroendocrinology
- Developmental Biology
- Pharmacology
Background:
- The regulation of prolactin (Prl) and growth hormone (GH) secretion in infant mammals is complex.
- Serotonin (5-HT) pathways are known to influence hormone release, but their specific roles in neonatal rats require elucidation.
Purpose of the Study:
- To investigate the role of the serotonin system in mediating the effects of 5-hydroxytryptophan (5-HTP) on prolactin and growth hormone release in 10-day-old rats.
- To differentiate the mechanisms underlying 5-HTP-induced prolactin and growth hormone responses.
Main Methods:
- Administration of 5-hydroxytryptophan (5-HTP) to infant rats.
- Pretreatment with serotonin receptor blockers (methysergide, metergoline).
- Administration of selective serotonin reuptake inhibitors (SSRIs) and blockade of dopaminergic/alpha-adrenergic receptors.
- Central sympathectomy using 6-hydroxydopamine (6-OHDA).
Main Results:
- 5-HTP administration increased plasma prolactin and growth hormone levels.
- Serotonin receptor blockers reduced the 5-HTP-induced prolactin rise but not the GH response.
- SSRIs potentiated the prolactin increase and reduced the GH release.
- Blockade of catecholaminergic systems reduced 5-HTP-induced GH release without affecting prolactin.
Conclusions:
- Prolactin release in response to 5-HTP in infant rats is mediated by the brain's serotonin system.
- Growth hormone release is linked to a non-specific activation of the catecholaminergic system by 5-HTP.
- These findings highlight distinct neurochemical pathways regulating neonatal prolactin and growth hormone secretion.
Abstract:
In 10 day-old female and male rats, administration of 5-hydroxytryptophan (5-HTP) induced a prompt elevation in plasma prolactin (Prl) and growth hormone (GH) levels. Pretreatment with 2 serotonin (5-HT) receptor blockers, methysergide (Meth) and metergoline (MCE), markedly reduced the 5-HTP-induced Prl rise but failed to alter the GH response to 5-HTP. Administration of 2 selective inhibitors of presynaptic 5-HT reuptake, 3-(p-trifluoromethylphenoxy)-N-methyl-3-phenyl-propylamine and chlorimipramine (CIM), potentiated the 5-HTP-stimulated Prl rise but significantly reduced the 5-HTP-induced GH release. Blockade of dopaminergic or alpha-adrenergic receptors by pretreatment with pimozide (Pim) or phentolamine (Phent), respectively, or central sympathectomy by intraventricularly (i.vt.) injected 6-hydroxydopamine (6-OHDA) were capable of reducing the 5-HTP-induced GH release without affecting the 5-HTP-induced Prl rise. These data indicate that in the infant rat the 5-HTP-induced Prl release is mediated via the brain 5-HT system and that a nonspecific activation of the catecholaminergic system is responsible for the GH response to the drug.