EFFECTS OF THE GABAERGIC DRUG, SODIUM VALPROATE, ON THE PROLACTIN RELEASE EVOKED BY PHARMACOLOGICAL STIMULI IN NORMAL WOMEN

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Abstract
Sodium valproate (DPA or sodium dipropylacetate), an anticonvulsant drug activating the endogenous GABAergic system, was administered orally at the dose of 400 mg to seventeen normal women 1 h before i.v. injections with 3 drugs which stimulate prolactin (PRL) release: TRH (200 .mu.g bolus; 6 subjects); domperidone (5 mg bolus; 6 subjects); and sulpiride (5 mg bolus; 5 subjects). DPA pretreatment significantly blunted PRL response to both domperidone and sulpiride injections without affecting the PRL response to TRH. In particular, the quantitative PRL secretion (areas under curves) following domperidone and sulpiride tests appeared significantly reduced after DPA treatment in comparison to placebo (P < 0.02 and P < 0.01 for domperidone and sulpiride, respectively). The pharmacological enhancement of the endogenous GABAergic system by DPA may blunt PRL response to both central and peripheral dopamine receptor blockade. These observations suggest that a GABAergic pathway inhibiting PRL secretion at the hypothalamic level competes, at least in part, with the dopaminergic system. Conversely, the lack of any effect of DPA on PRL response to TRH seems to suggest that pituitary TRH receptors are independent of any GABAergic control.