Hormonal modulation of central dopaminergic transmission

Central dopaminergic transmission is subjected to influences of various hormones of hypophyseal and extra-hypophyseal origin. Ablation of hypophysis prevents the supersensitivity of central dopamine receptors induced by chronic treatment with the dopamine receptor antagonist, haloperidol. Furthermore, hypophysectomized rats show a potentiation of hypomotility induced by low doses of the dopamine receptor agonist, apomorphine. Among the hypophyseal hormones, prolactin (PRL) seems to exert a modulatory activity on central dopamine transmission. Exogenous administration of PRL increases the density of dopamine receptors in intact and hypophysectomized rats. Furthermore, hyperprolactinaemic rats show alterations of the concentration and turnover of dopamine in various brain areas, and a potentiation of apomorphine-induced stereotypies. Endorphins related to gamma-endorphin also modulate central dopamine transmission. In particular, des-enkephalin-gamma-endorphin seems to interfere specifically with apomorphine-sensitive dopamine receptors. The administration of this endorphin is followed by a potentiation of hypomotility induced by low doses of apomorphine, and restores the sensitivity of hypophysectomized rats to these doses. The administration of estrogens also influences the sensitivity of central dopamine receptors. Depending on the doses, these hormones can potentiate or inhibit the dopaminergic neurotransmission in the brain.