Recent Progress in Hormone Research 

About: Recent Progress in Hormone Research is an academic journal. The journal publishes majorly in the area(s): Hormone & Receptor. It has an ISSN identifier of 0079-9963. It is also open access. Over the lifetime, 758 publications have been published receiving 77233 citations.

The neuroendocrine control of the menstrual cycle.

Abstract: Publisher Summary This chapter discusses the construction of a model of the neuroendocrine control system that governs the 28-day ovarian cycle of the rhesus monkey. This model has three basic components: the arcuate nucleus of the hypothalamus, the gonadotrophs of the pituitary gland, and the ovary. The arcuate nucleus is the central component of the control system. The gonadotrophs respond to this unvarying pulsatile gonadotropin releasing hormone (GnRH) stimulation by releasing pulses of follicle stimulating hormone (FSH) and luteinizing hormone (LH). Immature follicles respond to this unvarying gonadotropic stimulus by increasing in size and secreting increasing quantities of estradiol, which achieve maxima near mid-cycle. This process occupies approximately 14 days. The magnitude of the response to each GnRH pulse is modulated by estradiol acting directly on the gonadotrophs. The characteristic duration of the rhesus monkey ovarian cycle is thus determined by the duration of follicular development. This can occur in the presence of an absolutely unvarying pattern of hypophysiotropic stimulation.

Estrogen Actions Throughout the Brain

Abstract: Besides affecting the hypothalamus and other brain areas related to reproduction, ovarian steroids have widespread effects throughout the brain, on serotonin pathways, catecholaminergic neurons, and the basal forebrain cholinergic system as well as the hippocampal formation, a brain region involved in spatial and declarative memory. Thus, ovarian steroids have measurable effects on affective state as well as cognition, with implications for dementia. Two actions are discussed in this review; both appear to involve a combination of genomic and nongenomic actions of ovarian hormones. First, regulation of the serotonergic system appears to be linked to the presence of estrogen- and progestin-sensitive neurons in the midbrain raphe as well as possibly nongenomic actions in brain areas to which serotonin neurons project their axons. Second, ovarian hormones regulate synapse turnover in the CA1 region of the hippocampus during the 4- to 5-day estrous cycle of the female rat. Formation of new excitatory synapses is induced by estradiol and involves N-methyl-D-aspartate (NMDA) receptors, whereas downregulation of these synapses involves intracellular progestin receptors. A new, rapid method of radioimmunocytochemistry has made possible the demonstration of synapse formation by labeling and quantifying the specific synaptic and dendritic molecules involved. Although NMDA receptor activation is required for synapse formation, inhibitory interneurons may play a pivotal role as they express nuclear estrogen receptor-alpha (ERa). It is also likely that estrogens may locally regulate events at the sites of synaptic contact in the excitatory pyramidal neurons where the synapses form. Indeed, recent ultrastructural data reveal extranuclear ERalpha immunoreactivity within select dendritic spines on hippocampal principal cells, axons, axon terminals, and glial processes. In particular, the presence of ER in dendrites is consistent with a model for synapse formation in which filopodia from dendrites grow out to find new synaptic contacts and estrogens regulate local, post-transcriptional events via second messenger systems.

Protein glycation, diabetes, and aging.

Abstract: Biological amines react with reducing sugars to form a complex family of rearranged and dehydrated covalent adducts that are often yellow-brown and/or fluorescent and include many cross-linked structures. Food chemists have long studied this process as a source of flavor, color, and texture changes in cooked, processed, and stored foods. During the 1970s and 1980s, it was realized that this process, called the Maillard reaction or advanced glycation, also occurs slowly in vivo. Advanced glycation endproducts (AGEs) that form are implicated, causing the complications of diabetes and aging, primarily via adventitious and crosslinking of proteins. Long-lived proteins such as structural collagen and lens crystallins particularly are implicated as pathogenic targets of AGE processes. AGE formation in vascular wall collagen appears to be an especially deleterious event, causing crosslinking of collagen molecules to each other and to circulating proteins. This leads to plaque formation, basement membrane thickening, and loss of vascular elasticity. The chemistry of these later-stage, glycation-derived crosslinks is still incompletely understood but, based on the hypothesis that AGE formation involves reactive carbonyl groups, the authors introduced the carbonyl reagent aminoguanidine hydrochloride as an inhibitor of AGE formation in vivo in the mid 1980s. Subsequent studies by many researchers have shown the effectiveness of aminoguanidine in slowing or preventing a wide range of complications of diabetes and aging in animals and, recently, in humans. Since, the authors have developed a new class of agents, exemplified by 4,5-dimethyl-3-phenacylthiazolium chloride (DPTC), which can chemically break already-formed AGE protein-protein crosslinks. These agents are based on a new theory of AGE crosslinking that postulates that alpha-dicarbonyl structures are present in AGE protein-protein crosslinks. In studies in aged animals, DPTC has been shown to be capable of reverting indices of vascular compliance to levels seen in younger animals. Human clinical trials are underway.

The formation of estrogens by central neuroendocrine tissues

Abstract: 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 serum transport of steroid hormones.

Abstract: Publisher Summary This chapter discusses the serum transport of steroid hormones Steroid hormones are extensively bound to plasma proteins including albumin, corticosteroid binding globulin (CBG), and sex hormone binding globulin (SHBG) Because of its high concentration, albumin binding is important in determining the magnitude of the nonprotein bound or free fraction of a steroid in plasma The generally accepted model of steroid hormone action suggests that free steroid (in equilibrium with circulating binding proteins) diffuses passively through target cell membranes and binds to a soluble intracellular receptor The steroid-receptor complex apparently moves into the nucleus where it modifies the chromatin transcriptional activity which results in, among other things, altered levels of protein synthesis CBG has been differentiated from the intracellular glucocorticoid and progesterone receptors by its inability to bind synthetic glucocorticoids and progestins