In vivo Release of Dopamine, Luteinizing Hormone-Releasing Hormone and Thyrotropin-Releasing Hormone in Male Rats Bearing a Prolactin-Secreting Tumor

Abstract

The present study was concerned with the effects of a transplantable prolactin-secreting pituitary tumor (7315b) on the hypothalamic release of dopamine, luteinizing hormone-releasing hormone (LHRH) and thyrotropin-releasing hormone (TRH) in gonadectomized, adrenalectomized male rats bearing subcutaneously a testosterone capsule and a corticosterone pellet. Similar male rats not inoculated with tumor served as controls. The rats were studied 3–4 weeks after tumor inoculation, while they were anesthetized with urethane. Compared to the controls, prolactin levels in the tumor-bearing rats had increased 70-fold, whereas the levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) decreased to 20 and 27%, respectively. In tumor-bearing rats, the secretion of dopamine into hypophysial stalk plasma increased from 2.3 to 4.9 ng/h (p < 0.025), whereas that of LHRH decreased from 127 to 52 ph/h (p < 0.005). Since the use of urethane anesthesia may change quantitatively and qualitatively the effects of hyperprolactinemia, it was decided to study these effects on the in vivo release of LHRH, dopamine and TRH in conscious rats by a push-pull perfusion of the median eminence-arcuate nucleus area. Using this technique, it was found that in tumor-bearing rats the secretion of LHRH decreased from 20.0 to 9.8 pg/15 min·(p < 0.005), whereas that of dopamine increased from 118 to 246 pg/15 min (p < 0.025). The secretion of TRH was not altered by hyperprolactinemia (4.1 vs. 4.4pg/15 min). Thus, push-pull perfusion experiments in conscious, freely moving rats confirm what was found in hypophysial stalk blood obtained from rats under anesthesia, namely, that hyperprolactinemia stimulates dopamine release and inhibits LHRH release. This study also indicates the value of using conscious rats to determine simultaneously the in vivo output of several substances from the hypothalamus.

Prolactin regulation of testosterone secretion and testes growth in DLS rams at the onset of seasonal testicular recrudescence

“…Unlike in the rat (Voogt et al 1987, Koike et al 1991, PRL treatment does not appear to suppress hypothalamic GNRH secretion in sheep. Infusion of PRL into the third ventricle of the brain has little or no effect on episodic LH release in either rams (Lincoln & Tortonese 1997, Romanowicz et al 2004 or ewes (Curlewis & McNeilly 1991, Misztal et al 2005.…”

Influence of Thiouracil-induced Hypothyroidism on Adrenal and Gonadal Functions in Adult Female Rats.

“…Therefore, as long as the plasma concentrations of progesterone remain elevated, follicular growth will be retarded and small LH surges will occur. It also has been reported that hyperprolactinemia can reduce the secretions of LH [8,14] and GnRH [3,14,38]. Recent reports have suggested that CRH is probably involved in the suppressed secretion of LH during hyperprolactinemia [7,15].…”

In vivo Infusion of Adrenaline Stimulates Corticotropin‐Releasing Hormone‐Producing Neurons when given Centrally but not Distally

“…This negative result does not rule out the participation of the adrenergic innervation o f the M E in the regulation of the CRH-41 release into the portal system, especially as a 10-fold increase in the adrenaline concentration in the perfusate (10 -4 M ) resulted in a n apparent inhibition o f the CRH-41 release into the push-pull system. However, as n o true synaptic contacts have ever been demonstrated between catecholaminergic and CRH-41 -producing nerve terminals in the M E , a n d as a recent cxperiment with the same infusion procedure showed that at least 40% of the dopamine injected into the M E was actually trapped by M E nerve terminals (28), the physiological significance of high-dose infusions into the M E is questionable. Finally, it should be remembered that the CRH-41 concentrations measured in the push-pull perfusate under o u r experimental conditions stayed below the sensitivity threshold o f the RIA in several perfusion samples, which markedly reduces the precision of estimates of inhibitory regulations a t this far end of CRH-41-secretion neurons.…”