Prolactin is a protein hormone of the anterior pituitary gland that was originally named for its ability to promote lactation in response to the suckling stimulus of hungry young mammals. We now know that prolactin is not as simple as originally described. Indeed, chemically, prolactin appears in a multiplicity of posttranslational forms ranging from size variants to chemical modifications such as phosphorylation or glycosylation. It is not only synthesized in the pituitary gland, as originally described, but also within the central nervous system, the immune system, the uterus and its associated tissues of conception, and even the mammary gland itself. Moreover, its biological actions are not limited solely to reproduction because it has been shown to control a variety of behaviors and even play a role in homeostasis. Prolactin-releasing stimuli not only include the nursing stimulus, but light, audition, olfaction, and stress can serve a stimulatory role. Finally, although it is well known that dopamine of hypothalamic origin provides inhibitory control over the secretion of prolactin, other factors within the brain, pituitary gland, and peripheral organs have been shown to inhibit or stimulate prolactin secretion as well. It is the purpose of this review to provide a comprehensive survey of our current understanding of prolactin's function and its regulation and to expose some of the controversies still existing.

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Prolactin: Structure, Function, and Regulation of Secretion

Sex, Gender, and Pain: A Review of Recent Clinical and Experimental Findings

Central mechanisms of stress integration: hierarchical circuitry controlling hypothalamo-pituitary-adrenocortical responsiveness.

I. Introduction II. Mechanisms of Estrogen Action A. “Genomic” and “nongenomic” mechanisms B. Steroid hormone actions on gene expression C. Subtypes of estrogen receptors D. Steroid hormone actions on putative receptors on membranes E. Rapid actions of steroids on neuronal excitability F. Steroid hormone actions via second messengers G. Neuroprotective effects of estrogens H. Summary III. Areas of the Brain Affected Outside of the Hypothalamus A. Studies of hypothalamic and extrahypothalamic actions of estrogens B. Estrogens and the cholinergic system C. Estrogens and the serotonergic system D. Catecholaminergic neurons E. Spinal cord F. Hippocampus G. Glial cells, endothelial cells, and the blood-brain barrier H. Summary IV. Effects of Estrogens on Learning and Memory V. Estrogens, Neuroprotection, and Alzheimer’s Disease VI. Conclusions

Estrogen actions in the central nervous system.

Much of what I will discuss here today relates to brain differentiation in rodents. This subject was the interest of two outstanding British scientists, Geoffrey Harris and Peter MacDonald. Harris spent his scientific life and considerable intellectual powers observing and enlarging upon this very interesting phenomenon, which was originally described so brilliantly by Carroll Pfeiffer in 1936. Peter MacDonald was an outstanding young man who had already shown the key role of estrogens in central steroid actions by experiments such as the use of antiestrogens to block the action of androgens on brain differentiation, as described below. Geoffrey Harris’ life ended at the pinnacle and fruition of a career that included the elucidation of the neurovascular and chemical links between the brain and pituitary and the isolation of the LH releasing factor. Peter MacDonald's life and continued work were prematurely lost in the recent Paris air disaster; we can only guess what he might have contributed in years to come. However, both of these men left important scientific and intellectual legacies, part of which you have already heard about. If a man's work is what others judge him by, these two will stand up well to any test, any time. We owe them our gratitude and continued remembrance.

The formation of estrogens by central neuroendocrine tissues

In order to reveal the electrophysiological correlates of pulsatile LH release in ovariectomized rats, changes in multiple unit activity (MUA) in the arcuate nucleus (ARC), the medial preoptic area, t

Electrophysiological correlates of pulsatile gonadotropin release in rats.

The effects of electrical stimulation of the brain on the ovarian venous plasma concentrations of estradiol (E2) and progesterone (P) were investigated in female rats hypophysectomized and adrenalectomized at 1000 h on the day of proestrus. Stimulation was applied during the proestrous critical period under pentobarbital anesthesia, and contralateral ovarian venous blood was collected from 105–120 min after the stimulation. E2 and P concentrations, estimated by RIA, were significantly increased by stimulation of the medial basal prechiasmatic area (PVA), ventromedial hypothalamus, and areas in the mesencephalon and decreased by stimulation of the dorsal hippocampus, lateral amygdala, and mesencephalic areas. Ovarian blood flow was not affected by these stimulations. Ovarian nervotomy in the proestrous rats abolished E2 secretion induced by PVA stimulation. In intact proestrous rats, electrochemical stimulation of the PVA but not the preoptic suprachiasmatic area increased E2 and P concentrations, although...

Involvement of Ovarian Innervation in Steroid Secretion

The suprachiasmatic nucleus is suggested to be a generator of several circadian rhythms. In the present study, the suprachiasmatic nucleus was examined to determine whether it is involved in the generation of daily PRL and gonadotropin surges which are induced by estrogen administration in ovariectomized female rats. Blood samples were obtained at 3-h intervals for 24 h from individual animals with an indwelling atrial cannula. Subcutaneous injections of 50 μg estradiol benzoate into ovariectomized rats elicited pronounced surges of serum PRL, LH, and FSH, with a peak around 1800 h. Hypothalamic frontal deafferentation by a bayonet-shaped knife, which interrupted frontal afferents to the medial basal hypothalamus at the retrochiasmatic level, abolished the surges of PRL and gonadotropins. In rats with large lesions of the suprachiasmatic nuclei (destruction of more than 50% of the bilateral nuclei), the characteristic PRL surges were eliminated, whereas comparable PRL surges to those in sham-lesioned anim...

Loss of Estrogen-Induced Daily Surges of Prolactin and Gonadotropins by Suprachiasmatic Nucleus Lesions in Ovariectomized Rats*

Serum and pituitary LH and FSH were measured during the estrous cycle, following electrical stimulation of the medial preoptic area (MPO), medial part of the amygdala (AMYG), and dorsal hippocampus (H

Masazumi Kawakami

Papers

Electrophysiological correlates of pulsatile gonadotropin release in rats.

Involvement of Ovarian Innervation in Steroid Secretion

Loss of Estrogen-Induced Daily Surges of Prolactin and Gonadotropins by Suprachiasmatic Nucleus Lesions in Ovariectomized Rats*

Modulating effect of limbic structures on gonadotropin release.

Influence of electrical stimulation and lesion in limbic structure upon biosynthesis of adrenocorticoid in the rabbit.