Role of midbrain raphe nuclei in stress-, pentobarbital-, beta-endorphin-, or TRH-induced changes in plasma PRL levels of adult male rats.

Radiofrequency lesions of either the dorsal (LD) or the median (LM) raphe nuclei of male rat mesencephalon did not modify baseline levels of plasma prolactin (PRL). However, the PRL releasing effect of 30 min of immobilization stress was suppressed in LM rats and enhanced in LD rats. The PRL releasing effect of pentobarbital (PB, 50 mg/kg, IP) or of beta-endorphin (END, 15 micrograms/rat, intracerebroventricularly, ICV) also was enhanced in LD rats. TRH (10 micrograms/rat, ICV) administered concomitantly with either PB or END, antagonized the releasing effect of the former and enhanced the releasing effect of the latter in sham operated rats. Lesions of the raphe nuclei blocked the antagonizing effect of TRH, while the enhancing effect was heightened in LD rats. These results indicate that neurons originating in the raphe nuclei are not involved in the control of baseline plasma PRL levels. They indicate, furthermore, the existence of an inhibitory pathway originating in the dorsal raphe nucleus the suppression or activation of which is, at least partly, the mechanism of PB, END or TRH effects on PRL release. The PRL releasing effect of immobilization stress seems to be under a dual, mutually antagonistic control: activating through the median and inhibitory through the dorsal nucleus.