The Posterior Pituitary and Water Metabolism

Author(s):  
Willis K. Samson

The neurohypophysis, also called the posterior pituitary or neural lobe , is the ventral extension of hypothalamic tissue derived from a developmental down growth of the neuroectoderm forming the floor of the third cerebroventricle. It weighs approximately 0.10–0.15 g in humans and is well developed at birth, having been present since the fifth month of intrauterine life. In addition to containing glial elements called pituicytes, the posterior pituitary is composed of unmyelinated nerve fibers and axon terminals of neurons whose cell bodies reside primarily in the supraoptic and paraventricular hypothalamic nuclei. These hypothalamo-neurohypophyseal fibers deliver the two primary posterior pituitary hormones, oxytocin (OT) and arginine vasopressin (AVP), to the neural lobe in association with specific proteins, the neurophysins, once thought to be carrier proteins but now known to be portions of the OT and AVP precursor molecules. The neurons produce either OT or AVP, and under some circumstances both, and recent studies indicate that in addition to one of these two hormones, other neuropeptides, such as corticotropin-releasing hormone (CRH) and nesfatin-1, and neurotransmitters are also produced in OT- or AVP-containing cells. The phenomenon of colocalization of neuromodulatory agents has aroused a great deal of clinical interest in the role of neuropeptides such as OT and AVP in brain function. Both OT- and AVP-containing nerve fibers, originating in the supraoptic and paraventricular nuclei, project to a variety of other brain structures that are thought to be the sites of their observed central nervous system actions, and to the vicinity of the hypophyseal portal vessels in the median eminence. Release from these fibers of both OT and AVP explains the high levels of these hormones in portal blood and provides the framework for the actions of OT and AVP as modulators of anterior pituitary function. The arterial blood supply of the posterior pituitary is via the inferior (and to some degree the superior) hypophyseal arteries, which originate from the cavernous and postclinoid portions of the internal carotid artery.

2018 ◽  
Vol 2 ◽  
pp. 239821281881201 ◽  
Author(s):  
John A. Russell

Importance of the neuroendocrine brain for health and happiness has become clear since the 1960s. Foundations laid 100 years ago culminated in Geoffrey W Harris’s model of control by the brain of secretion of anterior and posterior pituitary gland hormones through, respectively, releasing factors secreted into the hypothalamic-hypophysial portal system, and directly from axon terminals into the systemic circulation. Confirmation, expansion and deepening of knowledge and understanding have followed increasingly sophisticated technology. This allowed chemical characterisation of the posterior pituitary hormones, oxytocin and vasopressin, the releasing factors, their receptors and genes, location of the neurosecretory neurons in the hypothalamus, and how their activity is controlled, including by neural and hormonal feedback, and how hormone rhythms are generated. Wider roles of these neurons and their peptides in the brain are now recognised: in reproductive and social behaviours, emotions and appetite. Plasticity and epigenetic programming of neuroendocrine systems have emerged as important features.


Pituitary ◽  
2021 ◽  
Author(s):  
Paul Eugène Constanthin ◽  
Nathalie Isidor ◽  
Sophie de Seigneux ◽  
Shahan Momjian

Abstract Purpose The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a well-known complication of transsphenoidal pituitary surgery, related to inappropriate secretion of arginine vasopressin (AVP). Its diagnosis is based on hyponatremia, with a peak of occurrence around day 7 after surgery and, to date, no early marker has been reported. In particular, copeptin levels are not predictive of hyponatremia in this case. Oxytocin (OXT) is secreted into the peripheral blood by axon terminals adjacent to those of AVP neurons in the posterior pituitary. Besides its role in childbirth and lactation, recent evidences suggested a role for OXT in sodium balance. The contribution of this hormone in the dysnatremias observed after pituitary surgery has however never been investigated. Methods We analyzed the urinary output of OXT in patients subjected to transsphenoidal pituitary surgery. Results While OXT excretion remained stable in patients who presented a normonatremic postoperative course, patients who were later diagnosed with SIADH-related hyponatremia presented with a significantly increased urinary secretion of OXT 4 days after surgery. Conclusion Taken together, these results show for the first time that urinary OXT output remains normally stable after transsphenoidal pituitary surgery. OXT excretion however becomes abnormally high on or around 4 days after surgery in patients later developing hyponatremia, suggesting that this abnormal dynamics of OXT secretion might serve as an early marker for transsphenoidal surgery-related hyponatremia attributed to SIADH.


2004 ◽  
Vol 78 (13) ◽  
pp. 6792-6798 ◽  
Author(s):  
Ellyn R. Mulcahy ◽  
Jason C. Bartz ◽  
Anthony E. Kincaid ◽  
Richard A. Bessen

ABSTRACT The presence of the prion agent in skeletal muscle is thought to be due to the infection of nerve fibers located within the muscle. We report here that the pathological isoform of the prion protein, PrPSc, accumulates within skeletal muscle cells, in addition to axons, in the tongue of hamsters following intralingual and intracerebral inoculation of the HY strain of the transmissible mink encephalopathy agent. Localization of PrPSc to the neuromuscular junction suggests that this synapse is a site for prion agent spread between motor axon terminals and muscle cells. Following intracerebral inoculation, the majority of PrPSc in the tongue was found in the lamina propria, where it was associated with sensory nerve fibers in the core of the lingual papillae. PrPSc staining was also identified in the stratified squamous epithelium of the lingual mucosa. These findings indicate that prion infection of skeletal muscle cells and the epithelial layer in the tongue can be established following the spread of the prion agent from nerve terminals and/or axons that innervate the tongue. Our data suggest that ingestion of meat products containing prion-infected tongue could result in human exposure to the prion agent, while sloughing of prion-infected epithelial cells at the mucosal surface of the tongue could be a mechanism for prion agent shedding and subsequent prion transmission in animals.


Science ◽  
1980 ◽  
Vol 207 (4429) ◽  
pp. 373-378 ◽  
Author(s):  
M. Brownstein ◽  
J. Russell ◽  
H Gainer

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