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The stress-response
Published in Herman Staudenmayer, Environmental Illness, 2018
Projections of CRH neurons from the hypothalamus to proopiomelanocortm-containing neurons in the arcuate nucleus in the brain stem promote the release of corticotropin and ß-endorphin from the latter, which serve to inhibit CRH secretion (Howlett and Rees, 1986). The neurons are connected to the LC-NE system and to the raphe nuclei that control the release of 5-HT. The release of the opioid proopiomelanocortin (POMC) from the arcuate nucleus affects learning and memory and the limbic system by its modulating effects on the LC-NE system and the raphe-5-HT system (Figure 9.3). The paraventricular nucleus (PVN) releases arginine vasopressin (AVP), which effects the release of ACTH, and ß-endorphin, which modulates the LC-NE system and the raphe-5-HT system.
Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
It was once believed that a neuron released only one neurotransmitter, as embodied in Dale’s Principle. It is now well-established that a neuron may release more than one neurotransmitter, a phenomenon referred to as neurotransmitter corelease. It was previously mentioned that multiple neuropeptides may be released from the same vesicle. Moreover, a neuron may corelease neuropeptides and small-molecule neurotransmitters or more than one small-molecule neurotransmitter. The vesicles for coreleased neurotransmitters can be found in the same synaptic bouton or in different locations. For example, GABA is coreleased with the neuropeptide somatostatin by neurons in the hippocampus and with neuropeptide Y in the arcuate nucleus. Dopamine is released with the neuropeptide glucagon-like peptide-1 in the nucleus accumbens, located in the basal forebrain, and is anatomically part of the basal ganglia (Section 12.2.3). Neurons in the tuberomammillary nucleus in the posterior hypothalamus corelease histamine, GABA, and the neuropeptides galanin, enkephalin (an opioid), and substance P. Retinal amacrine cells corelease GABA and ACh from different vesicle populations, subserving different physiological functions. ATP and GABA are coreleased in dorsal horn and lateral hypothalamic neurons. Glycine and GABA are coreleased by spinal interneurons and by cerebellar Golgi and Lugaro cells (Section 12.2.4.3). Dopamine and glutamate are coreleased by neurons in the ventral tegmental area (VTA) of the midbrain, and serotonin and glutamate are coreleased by neurons of the dorsal raphe nucleus in the brainstem (Section 12.2.5.2).
Nanobiosensors
Published in Vinod Kumar Khanna, Nanosensors, 2021
Why is it necessary to develop biosensors for these analytes? Because dopamine (DA), C6H3(ΟH)2–ΟH2–CH2–ΝH2, uric acid (UA), C5H4N4O3, and ascorbic acid (AA), C6H8O6, are three important biomolecules, which are widely distributed in the body of many mammals, and exhibit vital physiological functions, such as message transfer (communication) in the brain and in defense of the body against disease. DA, one of the major catecholamines, belongs to the family of excitatory chemical neurotransmitters. It is a biogenic (produced by living organisms or biological processes) amine, synthesized in the hypothalamus (the part of the brain that lies below the thalamus), in the arcuate nucleus, the caudad (toward the tail or posterior end of the body), and various areas of the central and peripheral nervous systems. Its concentration is of great consequence in the function of central nervous, renal, hormonal, and cardiovascular systems. Because extreme abnormalities of DA level are warning signs of several diseases, such as schizophrenia and Parkinson’s disease, the determination of the concentrations such compounds in real biological samples and the identification of changes in neurotransmission that correlate the behavioral states of animals are obvious targets in neurochemical studies, i.e., study of the chemical composition and processes of the nervous system and the effects of chemicals on it. Thus, it is important to develop sensitive, fast, and specific methods for the detection of DA, UA, and AA (Huang et al. 2008).
The interactions of diet-induced obesity and organophosphate flame retardant exposure on energy homeostasis in adult male and female mice
Published in Journal of Toxicology and Environmental Health, Part A, 2020
Gwyndolin M. Vail, Sabrina N. Walley, Ali Yasrebi, Angela Maeng, Kristie M. Conde, Troy A. Roepke
Homeostatic regulation of feeding behaviors and energy balance is a complex system but predominantly controlled via neuroendocrine pathways originating in the hypothalamus (Waye and Trudeau 2011). Briefly, the hypothalamus consists of multiple nuclei in which discrete neuronal subgroups communicate with each other to integrate peripheral indicators of energy states (Williams et al. 2001). With emotional and reward inputs from the limbic forebrain, the hypothalamus synthesizes feeding drive and communicates with the hindbrain for execution (Berthoud 2002; Grill and Hayes 2012). Within the hypothalamus lies the arcuate nucleus (ARC) which sits adjacent to a leaky portion of the blood-brain-barrier, and thus its neurons are in a unique position to directly sense energy state through peripheral signals such as glucose, insulin, leptin, and ghrelin (Saper, Chou, and Elmquist 2002; Schwartz et al. 2000). ARC neurons express receptors for these molecules, and their combined inputs to the paraventricular nucleus (PVN) and lateral hypothalamus (LH) help dictate food intake (Arora and Anubhuti 2006; Nahon 2006). Because hypothalamic control of energy homeostasis is highly regulated through hormone signaling pathways including estrogen receptor (ER) α and peroxisome proliferator-activated receptor (PPAR) γ (Garretson et al. 2015; Mauvais-Jarvis, Clegg, and Hevener 2013; Roepke et al. 2011; Sarruf et al. 2009), any EDC, such as OPFRs, that interact with these receptors may disrupt the complex balance of these pathways, sensitizing the system to metabolic disorders such as obesity and diabetes.