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Hypothalamic Neuroendocrine Regulation
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Our knowledge of hypothalamic neuroendocrine control emerged with the development of the neurobiology of neurosecretion.2 In the following years, the biochemical isolation and identfication of the hypothalamic neuropeptides enabled investigators to study the factors that participate in the regulation of the synthesis and release of the hypothalamic neuropeptides.
SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
ADH synthesis occurs in the cell bodies of the magnocellular neurones in the supraoptic (5/6) and paraventricular nuclei (1/6) of the hypothalamus. From there, ADH is transported down the axons of these neurones to their endings in the posterior pituitary (neurohypophysis or pars nervosa) where they are stored as secretory granules prior to release. Release is controlled directly by nerve impulses passing down the axons from the hypothalamus; this process is known as neurosecretion.
Stimulus-Secretion Coupling: Receptors
Published in Stephen W. Carmichael, Susan L. Stoddard, The Adrenal Medulla 1986 - 1988, 2017
Stephen W. Carmichael, Susan L. Stoddard
The effect of muscarine on neurosecretion from PC12 cells was studied by Rabe, DeLorme and Weight (1987). When PC12 cells were exposed to muscarine, the cells responded rapidly with increases in intracellular inositol triphosphate level and intracellular calcium and release of stored transmitter. These phenomena were blocked by a muscarinic antagonist but were unaffected by a nicotinic antagonist. These and other results suggest that the muscarine-stimulated release of neurotransmitter may be associated with an inositol triphosphate-induced mobilization of intracellular calcium.
The urocortin peptides: biological relevance and laboratory aspects of UCN3 and its receptor
Published in Critical Reviews in Clinical Laboratory Sciences, 2022
Norah J. Alghamdi, Christopher T. Burns, Roland Valdes
Historically, the concept of neurosecretion in stress responses began in the late 1930s, when Dr. Hans Selye, the founder of the stress theory, postulated that a “first mediator” excreted during stress can stimulate the discharge of adrenocorticotropic hormone (ACTH) [32]. In 1955, Saffran et al. first reported this mediator as CRH [34]. These discoveries set the stage for understanding the entire family of CRH-related peptides and their receptors. In 1995, Vaughan et al. discovered a novel peptide similar in its structure and function to urotensin and CRH in rat brains [18]. This novel peptide was later named urocortin 1 (UCN1). Two additional urocortins were identified in 2001 and named urocortin 2 (UCN2, described by Reyes et al. [17]), and urocortin 3 (UCN3, described by Lewis and Hsu [1,5]). UCN3, first identified as a neuropeptide expressed in the central nervous system, was subsequently discovered in peripheral tissues. Although this peptide is the least well-studied of the three, it has interesting biological functions of relevance to laboratory medicine.
Neuroprotective effects of natural compounds on neurotoxin-induced oxidative stress and cell apoptosis
Published in Nutritional Neuroscience, 2022
Bo Chen, Jingjing Zhao, Rui Zhang, Lingling Zhang, Qian Zhang, Hao Yang, Jing An
RNS refer to NO and molecules derived from NO, such as ONOO− and NO•. RNS are important factors for the generation of oxidative stress. In mitochondria, NO is produced from L-arginine in a catalytic reaction mediated by NOS, which has three isoforms: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). NO is implicated in many important processes in the CNS, including the regulation of synaptic plasticity, sleep-wake cycle, neurosecretion, and cerebral blood flow. In general, physiological amounts of NO are neuroprotective, while higher concentrations are obviously neurotoxic. The excessive release of NO impairs mitochondrial function and acts on neighboring cells, damaging lipids, proteins and nucleic acids, thus affecting cell metabolism and survival[14]. The reactive species can react with each other to produce more active forms, such as the free form of NO reacts with O2−• to produce ONOO− or peroxynitrite radical (ONOO•)[15]. ONOO− can be rapidly decomposed into HO•, nitrogen dioxide radical (NO2•), and nitryl cation (NO2+). All of them can damage nerve cells[16].
Rat hippocampal CA3 neuronal injury induced by limb ischemia/reperfusion: A possible restorative effect of alpha lipoic acid
Published in Ultrastructural Pathology, 2018
Ola A. Hussein, Amel M. M. Abdel-Hafez, Ayat Abd el Kareim
In the present study, pyramidal neurons of I/R groups occasionally contained large multivesicular bodies (MVBs) that contained numerous small internal vesicles enclosed within a single outer membrane. These large MVBs were especially observed in the degenerating electron dense shrunken neurons. It seems likely that the formation of these large vesicular structures was closely associated with perikaryal condensation and neuronal degeneration. Neuronal MVBs perform important functions in the neuronal cytoplasm involving regulation of the expression of receptor surface and exosome release, neurosecretion, signal termination, and clearance of toxins and unnecessary proteins via degradation or export to the extracellular space or neighboring cells.38 According to Clarke,39 the dead neuronal cells have been shown to undergo intense endocytosis, which serves to reduce the area of the plasma membrane. Increase in MVB size and/or number appeared to be a general adaptive response of neurons to injury by sequestrating aberrant proteins.40