RESTRAINT STRESS ENHANCES THE GENE-EXPRESSION OF PROLACTIN RECEPTOR LONG FORM AT THE CHOROID-PLEXUS

Hormonal control of brain functions is considered to be important in t he tolerance of stress, and it is now established that stress elevates serum PRL levels in male or cycling female rats. To investigate wheth er or how serum PRL acts on the brain during exposure to stress, we an alyzed serum PRL levels and the gene expression of brain PRL receptors in rats subjected to restraint stress in the water (RSW). The serum P RL concentration was remarkably increased within 30 min in the rats by exposure to RSW and decreased to the initial level after 4 h of RSW, remaining at this level for up to 7 h of RSW. After the rats were rele ased from the stress, the serum PRL level was significantly lowered in 6 h. Ribonuclease protection assay and in situ hybridization analysis revealed that messenger RNA (mRNA) expression for the long form PRL r eceptor [PRL-R(L)] was remarkably induced in the rat choroid plexus in 2 h of RSW. The high expression level of PRL-R(L) mRNA in the region was reduced after the rats were released from the stress. PRL-R(L) mRN A expression in the hypothalamus was at lower levels than those in the choroid plexus before and during the RSW treatment. The short form PR L receptor mRNA expression in the rat brain was considerably lower tha n expression of the long form receptor mRNA before or during RSW. The results indicated that the restraint stress caused a rapid increase in serum PRL and induced the gene expression for PRL-R(L) in the choroid plexus, suggesting stress-induced and choroid plexus PRL-R(L)-mediate d transport of serum PRL into the cerebrospinal fluid.