Although there is a large body of evidence linking cocaine use with central dopamine function, little is known about the direct or indirect effects of cocaine on the release of hormones from the anterior pituitary. The release of prolactin (PRL) is inhibited by dopamine originating from a discrete population of hypothalamic neurons. Thus, prolactin release is an indirect measure of dopamine release. We have found that rats receiving daily i.v. infusions of cocaine are mildly hyperprolactinemic before the daily session of cocaine as early as 5-10 days after initiation of the treatment. Furthermore, PRL is decreased markedly at the end of the infusion period. This persistent effect appears to be related to the ability of cocaine to block the uptake of released dopamine and a possible decrease in the ability of the neuron to release more dopamine in the absence of cocaine. In contrast, dopamine plays little if any role in the normal release of growth hormone (GH) from the anterior pituitary. Thus, cocaine does not affect the peripheral concentrations of GH unless the release of this hormone is stimulated by serotonin. The ability of serotonin to release GH is diminished immediately after cocaine treatment, perhaps reflecting the loss of access to a readily-releasable pool of GH, a functional uncoupling of serotonin to its receptors on neurons that secrete growth hormone-releasing factor, or a desynchronization of the normal pulsatile circadian rhythm of the release of GH.
