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The Renin-Angiotensin System
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
Similar effects have been demonstrated using organ-cultured neurons from the supraoptic nucleus which showed concentration-dependent spiking activity when super-fused with angiotensin II.385 These responses to angiotensin II could be blocked by angiotensin-receptor antagonists such as [Cys8]-angiotensin II or [Sar1 Ile8]-angiotensin II. However, these compounds did not affect spiking initiated by glutamate or nicotine. These results suggest the presence of specific angiotensin II receptors in neurons of the supraoptic nucleus.
Biological Activities of Peptides in Brain Tissues
Published in Gerard O’Cuinn, Metabolism of Brain Peptides, 2020
The hypothalamus is the richest area of GAL immunoreactivity and shows the most similar interspecies pattern of distribution. In the rat, there is a prominent cluster of cells in the ventrolateral portion of the medial preoptic area (MPA). These cells, which also contain oxytocin, innervate the posterior lobe of the pituitary through the supraoptic-hypophyseal tract. Large numbers of GAL ir perikarya occupy the dorsal aspects of the anterior hypothalamus, starting at the level of the anterior commissure and continuing to the PVN. A large number of GAL ir cell bodies occur in the PVN, both in the magno- and parvicellular subdivisions. Some of the immunoreactive cells in the parvicellular subdivision project to the median eminence, brainstem and spinal cord. Certain GAL-ergic neurons in the arcuate nucleus innervate other GAL-ergic cells, providing a system of feedback regulation of GAL secretion in the portal circulation. The supraoptic nucleus including the retrochiasmatic portion, accessory magnocellular nuclei and dorsomedial nucleus contain a large number of intensely-stained cells. The densest accumulation of GAL ir fibers and terminals in the hypothalamus is found in the median eminence. The fibers in the external zone contact the capillaries of the portal system; in the internal zone, they project to the posterior pituitary, where GAL is released into the general circulation.
Hypothalamic Neuroendocrine Regulation
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
When release of neurohypophyseal hormones is required, the magnocellular neurons develop specific firing patterns.98 Oxytocin neurons can be characterized electrophysiologically by their synchronous high-frequency discharge during suckling, and vasopressin neurons by their asynchronous phasic activity.99 The release of oxytocin and vasopressin is triggered by central inputs to the supraoptic and paraventricular nuclei or directly by osmotic stimuli at cells of the supraoptic nucleus.100 At the level of the neurohypophysis, hormone release can be modulated by various neurotransmitters and neuropeptides. The modulatory factors are either colocalized and co-released with the vasopressin or oxytocin, or contained within separate transmitter endings.101 It is clear that magnocellular neurons contain numerous peptides. They are present in smaller amounts than vasopressin and oxytocin. The peptides include dynorphin, enkephalins, galanin, cholecystokinin, TRH, CRH, neuropeptide Y, and other uncharacterized proteins.102 The relative amounts of these co-packaged peptides vary under different physiological conditions.
Evaluating the efficacy of oxytocin for pain management: An updated systematic review and meta-analysis of randomized clinical trials and observational studies
Published in Canadian Journal of Pain, 2023
Anastasia A. Mekhael, Jennifer E. Bent, Jonathan M. Fawcett, Tavis S. Campbell, Aldo Aguirre-Camacho, Alison Farrell, Joshua A. Rash
Potentially complementary mechanisms exist through which the oxytocinergic system influences the perception of pain. Oxytocin released into the central nervous system is thought to play an important role in the modulation and transmission of pain signals.14,15 Animal models have indicated that oxytocin in regions of the brain such as the periaqueductal gray influence pain modulation through endogenous opiate peptides, an effect that is attenuated with the administration of oxytocin or opiate receptor antagonists.16 Similarly, the paraventricular spinal pathway projects oxytocin to the lamina of the dorsal horn,17,18 a structure in which most nociceptive primary afferent neurons terminate.19 Oxytocin in the dorsal horn activates a set of glutamatergic interneurons that result in GABAergic inhibition of pain transmitting Aδ- and C-fibers at nociceptive-specific and wide dynamic range neurons.14,20,21 There is also evidence that oxytocin is released from the supraoptic nuclei of the hypothalamus into the periphery, where it has indirect antinociceptive effects.22 Importantly, oxytocin does not cross the blood–brain barrier, with an estimated perfusion of 1% to 2%,23 and peripheral oxytocin seems unlikely to exhibit central effects.
Regional shape alteration of left thalamus associated with late chronotype in young adults
Published in Chronobiology International, 2023
Cheng Xu, Hui Xu, Zhenliang Yang, Chenguang Guo
Many studies have used magnetic resonance imaging (MRI) to examine the relationship between chronotypes and brain structure. EC individuals exhibited higher regional gray matter density in the bilateral orbitofrontal cortex and hypothalamic area, while LC individuals exhibited higher regional gray matter density in the precuneus and left posterior parietal cortex (Takeuchi et al. 2015). They suggest that reduced gray matter density in bilateral hypothalamic clusters around the supraoptic nucleus in LC individuals may be associated with reduced function in these areas, and that damage and dysfunction in these nuclei typically results in more nocturnal behavior versus more daytime sleep (Edgar et al. 1993). Moreover, it has also been found that LC individuals showed reduced gray matter volume in the lateral occipital cortex, left anterior insula, and right pars triangularis (Rosenberg et al. 2018). This study suggests that although the neural mechanisms underlying chronotype differences remain to be elucidated, it is also hypothesized that cortical thickness, cortical surface area, and cortical folding characteristics are likely to be important in accounting for individual schedule pattern differences. Another study examined potential risk factors for depression and found that night preferences were associated with localized atrophy of the right hippocampus, increasing the risk of depression (Horne and Norbury 2018).
Effects of Nesfatin-1 on Food Intake and Hyperglycemia
Published in Journal of the American College of Nutrition, 2020
Nesfatin-1 is a recently described anorexigenic peptide, which may be involved in weight loss, malnutrition, and the regulation of appetite (3). Nesfatin-1 contains 82 amino acids derived from nucleobindin-2 (NUCB2), a precursor peptide (4–6). Nucleobinbin-2 mRNA (NUCB2 mRNA) is produced in different areas of the brain and is involved in the regulation of nutrition. These areas of the brain are brain stem, paraventricular nucleus (PVN), supraoptic nucleus (SON), arcuate nucleus (ARC), lateral hypothalamic area, and dorsal vagal complex (6,7). Nesfatin-1 is released from endocrine cells such as gastric and intestinal mucosal cells and pancreatic beta cells and is present in peripheral tissues such as muscle and adipose tissues (6,8,9). It can cross the blood–brain barrier (3, 6,10). Endogenous and peripheral administration of nesfatin-1 can reach the brain and inhibit eating behavior. Nesfatin-1 is capable of inhibiting food intake when administered subcutaneously and can sustain its anorexigenic effects 14 hours after injection. Peripheral administration of nesfatin-1 may decrease food intake (7,11). Nesfatin-1 is an inhibitory factor on appetite and a regulator of energy balance that reduces the increase in body weight (9,12).