Paraventricular Nucleus Mediates Prolactin Secretory Responses to Restraint Stress, Ether Stress, and 5-Hydroxy-L-Tryptophan Injection in the Rat*

Publisher Website
Google Scholar
Abstract
The role of the paraventricular nucleus (PVN) in mediating acute stimulatory PRL responses was investigated in conscious male rats. Electrolytic lesions, verified histologically at autopsy, were stereotaxically made in the PVN region, and sham lesions were made in control rats. Blood was obtained through a chronically indwelling catheter in the right atrium. PVN-lesioned (PVL) rats showed significantly lower T3 levels 1 week after surgery (< 34.4 ng/dl) compared with sham (mean .+-. SEM, 91.2 .+-. 5.0 ng/dl) and intact (86.8 .+-. 2.0 ng/dl) animals, verifying a lesion in the PVN. T3 was restored to normal (95.6 .+-. 1.8 ng/dl) by daily sc administration of T4 (10 .mu.g/kg BW) for at least 4 days before the day of the experiments. Basal PRL levels in PVL rats did not differ significantly from those in control or sham-lesioned animals. In response to restraint stress, plasma PRL levels of PVL rats did not rise, in contrast to marked elevation in PRL in sham and intact rats [PRL level (mean .+-. SEM; nanograms per ml), basal to peak: PVL, 4.3 .+-. 0.3 to 4.5 .+-. 0.4; sham, 4.5 .+-. 0.5 to 47.0 .+-. 4.1; intact, 4.0 .+-. 0.3 to 46.3 .+-. 4.9]. PVL also resulted in the complete inhibition of PRL secretion induced by 30-min inhalation of ether (basal to peak: PVL, 3.3 .+-. 0.3 to 4.5 .+-. 0.2; sham, 5.7 .+-. 0.8 to 19.9 .+-. 0.9; intact, 3.3 .+-. 0.4 to 27.9 .+-. 4.0). The stimulatory effect on plasma PRL in sham and intact rats by one iv bolus injection of the serotonin precursor 5-hydroxy-L-tryptophan (5-HTP; 10 mg/kg BW) was completely abolished in PVL animals (basal to peak: PVL, 3.7 .+-. 0.6 to 5.2 .+-. 1.4; sham, 6.7 .+-. 0.6 to 36.0 .+-. 0.5; intact, 4.1 .+-. 1.2 to 33.3 .+-. 3.2). In contrast to the marked alteration in PRL regulation, PVL rats exhibited a typical ultradian rhythm of plasma GH secretion during a 6-h observation period and increased release of GH induced by iv injection of 5-HTP [GH (nanograms per ml), basal to peak; PVL, 4.5 .+-. 0.6 to 21.0 .+-. 4.9; sham, 3.7 .+-. 0.3 to 18.4 .+-. 4.4; intact, 2.9 .+-. 0.1 to 17.8 .+-. 3.5]. These findings indicate that PRL responses to stress and to serotonin act through the PVN, the site of origin of several putative PRL-releasing factors. Furthermore, since the arcuate region, which mediates GH secretion and includes the tuberoinfundibular dopaminergic system, was demonstrated to be both functionally and histologically intact in PVL animals, we hypothesize that disinhibition of tonic dopamine release is not a significant factor in causing acute PRL secretion during stress or in response to serotonin.