Distribution and Characteristics of Brain Dopamine
Nira Ben-Jonathan in Dopamine, 2020
The pituitary gland is suspended from the median eminence by the infundibulum (pituitary stalk) and is nested within the sella turcica of the sphenoid bone of the skull. The median eminence is one of the seven areas of the brain called circumventricular organs, which have fenestrated capillaries and are therefore devoid of the BBB [37]. As illustrated in Figure 3.9, the median eminence is composed of three distinct zones: ependymal, internal, and external. The ependymal zone forms the floor of the third ventricle and has several specialized features, including tight junctions between adjacent cells and highly specialized cells, the tanycytes. Tanycytes are glial-like cells that extend protrusions and microvilli into the cerebrospinal fluid (CSF) at their ventricular surface and long cytoplasmic processes into the body of the median eminence. Tanycytes are exposed to CSF from the third ventricle and also have an access to circulating hormones and various metabolites through the fenestrated capillaries [38]. Some of the tanycytes act as conduits for trafficking certain molecules into the brain parenchyma, while others act as neural stem/progenitor cells that supply the postnatal and adult hypothalamus with new neurons. During embryonic development, tanycytes also serve as a scaffolding for axons that enter the median eminence, guiding them to their ultimate destination in the external zone.
Influence of Ovarian Hormones on the Regulation of Luteinizing Hormone and Prolactin Release by Angiotensin II
Craig A. Johnston, Charles D. Barnes in Brain-Gut Peptides and Reproductive Function, 2020
In terms of LH, it is clear that the facilitatory effects of AII are mediated by norepinephrine which then acts, probably directly, at LHRH neurons. The AII-norepinephrine interaction apparently occurs within the anterior hypothalamus. Future experiments are necessary to determine where, for example, neurotensin and oxytocin fit into this scheme. Do they act via norepinephrine, the opioids, or directly on the LHRH neuron? Do they act in parallel or in sequence with AII to affect LHRH release? Do they act at the anterior hypothalamus or at the median eminence? Similar questions can be raised regarding AII and prolactin. Although we have evidence that the suppressive effects of AII on prolactin are mediated by dopamine, we do not know where this interaction occurs or whether AII acts directly on dopamine neurons (cell bodies or terminals), or via an intervening substance? Hopefully, the work presented both in this chapter and this volume will facilitate answers to these questions and ultimately provide a map to understand brain and pituitary peptide control over anterior pituitary hormone secretion.
Psychoneuroimmunology, Stress and Infection
Herman Friedman, Thomas W. Klein, Andrea L. Friedman in Psychoneuroimmunology, Stress, and Infection, 2020
It is not yet clear how IL-1 or other cytokines affect the brain. The molecule (M.Wt. 17,500) appears too large to readily cross the blood-brain barrier,92 but it may act directly on the organum vasculosum laminae terminalis (OVLT)93 or the median eminence.80 It has been suggested that there is a specific brain uptake system for IL-1,94 but the function of such a system has not been clearly established. Curiously, binding sites for IL-1 have been demonstrated in the brains of mice, but not rats.95,96 IL-1 does not appear to be present in the normal healthy brain.72,97 It does appear, however, when the brain is infected or lesioned. The blood-brain barrier is then breached allowing invasion of macrophages from the periphery, which then proliferate in the CNS as microglia which can synthesize IL-1. The IL-1 acts as potent growth factor for astroglia, causing them to proliferate, sealing off the lesion and restoring the damaged blood-brain barrier.98 Thus IL-1 plays an important role in a classical pathological mechanism for protection of the brain.
One-week exposure to a free-choice high-fat high-sugar diet does not disrupt blood–brain barrier permeability in fed or overnight fasted rats
Published in Nutritional Neuroscience, 2019
M. Rijnsburger, U. A. Unmehopa, L. Eggels, M. J. Serlie, S. E. la Fleur
The delivery of blood-borne molecules like hormones and nutrients to the hypothalamus is restricted by the blood–brain barrier (BBB).1,2 The arcuate nucleus (Arc) of the hypothalamus lies adjacent to the third ventricle and is in close proximity with the median eminence (ME), a circumventricular organ with an incomplete BBB. Thus, the hypothalamus is in (in)direct contact with circulating molecules through the systemic circulation and through the cerebrospinal fluid (CSF). The brain–CSF barrier of the third ventricle is composed of tanycytes, specialized hypothalamic glia cells.3 The tanycytes at the floor of the third ventricle (β2 type) are unique, because they have direct access to the circulation via fenestrations of the BBB found at the ME. β1 tanycytes, present on the border between the ME and the Arc, form the ME-Arc barrier and thus allow the actual entrance of substances into the hypothalamus.4 Tight junction (TJ) complexes between adjacent tanycytes act as a physical barrier controlling the paracellular passage of substrates over the brain–CSF or ME–Arc barrier.5 These complexes consist of occludin, claudins, and junctional adhesion molecules, groups of transmembrane proteins important for intercellular adhesion. In addition, zonula occludens (ZO) proteins are intracellular TJ proteins and proposed to be scaffolding proteins that link the extracellular TJs to the actin cytoskeleton.5
Role of glucocorticoid negative feedback in the regulation of HPA axis pulsatility
Published in Stress, 2018
Julia K Gjerstad, Stafford L Lightman, Francesca Spiga
The hypothalamic–pituitary–adrenal (HPA) axis regulates circulating levels of glucocorticoid hormones (cortisol in humans, corticosterone in the rat and mouse; hereafter referred to as CORT) and is the major neuroendocrine axis regulating homeostasis in mammals. When stress activates the HPA axis the resultant increase in CORT prepares the body to cope with and recover from, the stressor. Glucocorticoids have a wide range of effects; they are involved in the regulation of metabolic processes, immune system, reproduction, behavior and cognitive functions (Cherrington, 1999; Chrousos, 1995; de Kloet, 2000; Macfarlane et al., 2008; McEwen, 2007; Munck et al., 1984). The main activator of the HPA axis is the neuropeptide corticotropin-releasing hormone (CRH), synthetized in the hypothalamic paraventricular nucleus (PVN). Upon activation, CRH is released into portal vessels of the median eminence to reach the anterior pituitary where it stimulates the synthesis and release of adrenocorticotropic hormone (ACTH) from corticotroph cells (Antoni, 1986; Vale et al., 1981). ACTH in turn is secreted into the blood circulation from where it reaches the adrenal cortex to stimulate the synthesis and secretion of CORT (Dallman et al., 1987).
Hypophysitis related to immune checkpoint inhibitors: An intriguing adverse event with many faces
Published in Expert Opinion on Biological Therapy, 2021
Maria V Deligiorgi, Charis Liapi, Dimitrios T Trafalis
The aforementioned mechanisms may rationalize the predilection of ir hypophysitis for the anterior pituitary. An alternative explanation for this predilection is the distinct vascularity of the anterior pituitary, which renders it more vulnerable to immunotherapy compared to the posterior pituitary. The anterior pituitary is the most richly vascularized mammalian tissue receiving 0.8 ml/gr/min from a portal circulation linking the median eminence of hypothalamus with the anterior pituitary. Arterial blood is supplied by the superior, middle, and inferior hypophysial artery branches of the internal carotid arteries. The pituitary stalk and the posterior pituitary are supplied directly from branches of the middle and inferior hypophysial arteries [27]. Contrary to the anterior pituitary that produces and secretes ACTH, LH/FSH, TSH, GH, PRL, the posterior pituitary secrets AVP stored in the distal axon terminals of the hypothalamic magnocellular neurons, the cell bodies of which synthesize AVP as a large precursor peptide [28].
Related Knowledge Centers
- Circumventricular Organs
- Hypophyseal Portal System
- Pituitary Stalk
- Tuber Cinereum
- Capillary
- Hypothalamus
- Optic Chiasm
- Cerebral Peduncle
- Blood–Brain Barrier
- Vascular Permeability