On the Role of the Central Serotoninergic System in the Regulation of the Secretion of Thyrotropin and Prolactin- Thyrotropin-Inhibiting and Prolactin-Releasing Effects of 5-Hydroxytryptamine and Quipazine in the Male Rat*

Pharmacological Evidence that Serotonergic Stimulation of Prolactin Secretion is Mediated via the Dorsal Raphe Nucleus

“…Moreover, inhibition of 5-HT synthesis by pre treatment with PCPA, blocked the prolactin stimulatory ef fect of PCA. These results are consistent with previous re ports that injection of serotonin into the third ventricle and systemic administration of 5-hydroxytryptophan both ele vate prolactin levels [7,28].…”

“…In contrast, median raphe lesions did not prevent the effect of PCA on plasma prolactin levels. In summary, these data support the hypothesis that release of serotonin increases prolactin secretion, in addition, these data suggest that serotonergic neurons in the dorsal raphe nucleus are part of a neural pathway which can mediate increases in prolactin se cretion.There is considerable pharmacological evidence sup porting the hypothesis that activation of the serotonergic pathways in the central nervous system results in increased prolactin secretion [1,[6][7][8][9][25][26][27][28], The majority of central serotonergic neurons originate in the dorsal and median raphe nuclei in the hindbrain [2][3][4][5]12] and project rostrally, innervating hypothalamic and rostral limbic and cortical areas [2,33,36.42.43].Since serotonin (5-HT) does not cross the blood-brain barrier [14], various pharmacological agents have been uti lized to examine the regulatory functions of the serotoner gic projections.DT-p-chloroamphetamine (PCA) is a drug which affects catecholamine neurotransmission [11,15,21,37,38,40] and has a biphasic effect on brain serotonin. In the initial few hours it causes a substantial release [18,30,41] followed by long-term inhibition of tryptophan hydroxylase, serotonin uptake, monoamine oxidase and depletion of serotonin stores [37,38].…”

Partial Characterization of a Neurotransmitter Pathway Regulating the in vivo Release of Prolactin

“…These include serotonin (5-HT) agonists [4][5][6], opioid peptides and morphine [7][8][9][10] and nicotine [11,12], It is presumed that nicotine and serotonergic ago nists stimulate receptors at synapses where acetylcholine and 5-HT, respectively, are the endogenous neurotrans mitters. Morphine releases prolactin by stimulating popiate receptors [13][14][15]; and here, (i-endorphin may be the endogenous transmitter, since it is the most potent of the opioid peptides tested in releasing prolactin.…”

Site-Dependent Action of Intracerebroventricular 5-Hydroxytryptamine on the Cold-Stimulated Thyrotropin Secretion in Male Rats

“…Only the action of 5-HT was blocked by methysergide, a 5-HT receptor antagonist. Injec tions were given into the third ventricle 1.3 mm behind the bregma [19], This site is 1.0 mm caudal to the one we have used for the anterior third ventricle in the present study. Blunting of the TSH cold response has also been observed after intracere broventricular infusions o f 5-HT and quipazine [26].…”