This review examines the effects of cocaine on the neuroendocrine system and summarizes findings from clinical studies of cocaine abusers and preclinical studies in rodents and rhesus monkeys. The effects of acute and chronic cocaine administration on anterior pituitary, gonadal, and adrenal hormones are described, and the functional consequences of chronic cocaine exposure are discussed. Many of cocaine's acute effects on the endocrine system are consistent with its actions as a monoamine reuptake inhibitor. Acute cocaine administration stimulates release of gonadotropins, ACTH, and cortisol or corticosterone and suppresses prolactin levels. It has been difficult to detect changes in basal levels of most hormones or alterations in hormone responsiveness to a challenge dose of cocaine or other agents after chronic cocaine treatment. Interpretation of clinical data is often complicated by polydrug abuse involving opiates and alcohol as well as cocaine. However, preclinical studies of the effects of chronic cocaine exposure on integrated neuroendocrine function have revealed disruptions of the estrous cycle in rats and the menstrual cycle in rhesus monkeys. Furthermore, the menstrual cycle disorders observed in rhesus monkeys parallel those reported in women who abuse cocaine. Much remains to be learned about cocaine's interactions with the endocrine system and the consequences of cocaine abuse for reproductive function.

Cocaine’s Effects on Neuroendocrine Systems: Clinical and Preclinical Studies

DURING the past decade, advances in diagnostic methods have changed the amenorrhea-galactorrhea syndrome from a relative medical curiosity to a well recognized and frequently diagnosed disorder. Before the availability of a radioimmunoassay for prolactin (PRL) and sophisticated radiographic methods, patients with amenorrhea-galactorrhea were characterized by eponymic designations. The spectrum of patients now recognized as having hyperprolactinemia and PRL-secreting tumors includes postpartum amenorrhea-galactorrhea described by Chiari et al. (1) and Frommel (2), spontaneous amenorrhea-galactorrhea described by Argonz and del Castillo (3), and the amenorrhea-galactorrhea syndrome with evidence of a pituitary tumor on conventional skull x-rays described by Forbes et al. (4). The refinement of the transsphenoidal surgical approach to exploration of the sella turcica and the knowledge that amenorrheagalactorrhea and infertility can be reversed by selective surgical excision of a pituitary tumor has created n...

Prolactin-Secreting Pituitary Tumors in Amenorrheic Women: A Comprehensive Study

The participation of the catechol aminergic system of the brain in the central regulation of gonadotropin (FSH and LH) and prolactin (PRL) release is now established in all mammalian soecies studied except in humans (39). That the tuberoinfundibuiar dopamine (DA) system functions as a hypothalamic PRL inhibitor by a direct action of the DA-receptor of the lactotrope, delivered by way of the hypophyseal portal system is unequivocally demonstrated (8,13,20,37,38, 53,54). By contrast, catecholamines which influence gonadotropin secretion appear to operate by way of a central site(s), affecting the peptidergic neuron that produces LRF (19,21,22,25,35,41,48,51). Through the use of immunohistochemistry, Fuxe and associate and Lofstrom et al. have demonstrated a morphological relationship which serves as a basis for the interaction between DA, norepinephrine (NE), and LRF nerve terminals in the median eminence of the rat (18,19,35). Recently, axo-axonic contact of LRF and DA terminals was demonstrated in close proximity to the portal vessels of the rat median eminence suggesting the synaptic influence of DA on the release of LRF into the portal system (1a, 40).

Studies of the Role of Dopamine in the Control of Prolactin and Gonadotropin Secretion in Humans

Cocaine stimulates the release of hypothalamic–pituitary–adrenal (HPA) and gonadal hormones in men and women, in nonhuman primates, and in rodents. Repeated activation of the HPA axis and the hypothalamic–pituitary–gonadal (HPG) axis by cocaine can interfere with the complex feedback regulation of these systems and profoundly disrupt reproductive function. Moreover, stimulation of HPA- and HPG-axis hormones may modulate cocaine's behavioral and reinforcing effects under some conditions. Sex and menstrual/estrous cycle phase each appear to influence the abuse-related effects of cocaine. This chapter examines the reciprocal interactions between the acute and chronic effects of cocaine, HPA- and HPG-axis hormones, and cocaine-related behaviors. An increased understanding of neurobiology of cocaine and its interactions with sex and neuroactive hormones may lead to new approaches to treatment of cocaine abuse.

Cocaine, Hormones, and Behavior: Clinical and Preclinical Studies

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The effect of l-dopa and chlorpromazine on prolactin and growth hormone secretion in normal women

Glucagon secretion in late pregnancy and the puerperium