EFFECT OF CASTRATION AND CASTRATION WITH HORMONE REPLACEMENT ON THE PLASMA PROLACTIN RESPONSES TO NEUROENDOCRINE CHALLENGE WITH IV MCPP IN THE MALE-RAT FOLLOWING A LOW TRYPTOPHAN DIET

Previous studies have shown that castration increased brain 5-HT synth esis and that sex steroid hormone treatment can reverse this effect. T ryptophan (TRP) depletion has been shown to reduce brain 5-HT synthesi s and to cause the post-synaptic 5-HT receptors to up-regulate. We hav e studied the effects of castration and hormone replacement on the pro lactin responses to neuroendocrine challenge with the post-synaptic 5- HT agonist, m-chlorophenylpiperazine (m-CPP) in male rats on a low TRP diet. Intact rats on a low TRP diet for 6 days showed significantly e nhanced PRL reponses to mCPP as compared to intact rats on a complemen tary control diet. Animals castrated 20 days prior to neuroendocrine t esting and on a low TRP diet demonstrated a loss of the enhanced PRL r esponse to mCPP. The enhanced PRL response was restored by treatment w ith 25 mg/kg of testosterone proprionate (TP) 24 h prior to testing. R ats treated with oestradiol benzoate (OB) from initial castration, sho wed significantly raised basal PRL concentrations but did not show enh anced PRL responses to mCPP in animals on either a low TRP diet or on a control diet as compared to castrated controls. It is suggested that castration increases brain 5-HT in these animals which leads to a dow n-regulation of post-synaptic 5-HT receptors. When the animals are the n subjected to a low TRP diet for 6 days, a reduction in brain 5-HT sy nthesis occurs, causing a rebound up-regulation of the 5-HT receptors and therefore the end effect is a stalemate between the two initial ef fects resulting in the loss of the enhanced response. TP but not OB tr eatment in these animals restores the enhanced PRL response to mCPP by reducing brain 5-HT synthesis and returning the postsynaptic 5-HT rec eptors to a state of up-regulation.