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Psychopharmacology in Aviation
Published in Carrie H. Kennedy, Gary G. Kay, Aeromedical Psychology, 2013
Bradford C. Ashley, Gary G. Kay
Classic models assert that mental illness is due to structural abnormalities in the brain, neuronal dysfunction, and/or neurochemical imbalances. However, recent research, for example into the genetics of mental illness, has shown that these models are overly simplistic and fail to take into account the complexity of mental illness (Kohli et al. 2011). Regardless, current treatment of mental illness is based on restoring balance to several key neurotransmitters believed to be central in the pathogenesis of psychiatric illness. Most of this work dates back to the monoamine hypothesis of depression and the dopamine hypothesis of schizophrenia (Howes and Kapur 2009). These key transmitters include norepinephrine (NE), serotonin (5HT), and dopamine (DA). It was thought that psychiatric medications worked by simply changing the synaptic concentrations of these neurotransmitters in key areas of the brain. This is a helpful model but again overly simplistic. The model does explain some of the side-effects that are seen when these substances activate receptors outside the central nervous system (CNS). For example gastrointestinal (GI) distress can be caused by activating serotonin receptors found in the GI tract. It is now believed that the key neurotransmitters merely act as intermediate steps in more complex changes at the cellular level. The precise mechanism of action of most psychotropic medications has yet to be fully determined.
Drugs for Treatment of Neurological and Psychological Conditions
Published in Richard J. Sundberg, The Chemical Century, 2017
The amphetamines and analogs act by releasing noradrenaline and dopamine in the hypothalamus and have a powerful effect of inhibiting appetite (anorexigens). The hypothalamus has receptors for neuropeptides that either enhance (orexigenic) or suppress (anorexigenic) appetite. Norephedrine was available over-the-counter in the United States and Europe as its hydrochloride salt under brand names such as Monydrin, Proin, and Propalin. It was withdrawn in 2000 as a result of studies that indicated an increased risk of hemorrhagic stroke. An amphetamine analog, aminorex, was introduced as an anorexigen in Europe in the 1960s. It was subsequently linked to an increased incidence of primary pulmonary hypertension and was withdrawn from the market in the 1970s. Phentermine was granted FDA approval in the United States in 1959. Fenfluramine was approved in 1973. They were approved only for treatment of obesity and for short-term use. These drugs act by stimulating release of serotonin and activating serotonin receptors. These effects suppress appetite through the effect of serotonin on cerebral centers. During the 1990s, the use of amphetamine weight-loss drugs grew rapidly. The pure active enantiomer of fenfluramine, called dexfenfluramine and sold as Redux, was approved for use in 1995, on a close split vote of the FDA advisory panel. The approved use was for short-term treatment of obesity. Approval was withdrawn in 1997. The combination of fenfluramine and phentermine, known as fen-phen, was introduced in 1992, although the combination was never approved by FDA. It is believed that more than 8 million people, mostly women, received prescriptions. The structures of these drugs are shown in Scheme 17.9.
The Nature of Being Human
Published in Beverly G. McCarter, Brian E. White, Leadership in Chaordic Organizations, 2016
According to Damasio, a large number of serotonin receptors reside in the ventromedial sector of the prefrontal cortex as well as in the amygdala. Serotonin is one of the main neurotransmitters that affect social behavior. In primates it inhibits aggressive behavior and favors social behavior. This research points to an interactive connection between the ventromedial prefrontal cortices and the amygdala, relating these regions to social behavior that is affected by flawed decision making.
Epigenotoxicity: a danger to the future life
Published in Journal of Environmental Science and Health, Part A, 2023
Farzaneh Kefayati, Atoosa Karimi Babaahmadi, Taraneh Mousavi, Mahshid Hodjat, Mohammad Abdollahi
Recent information on the relationship between epigenetics and eating disorders is limited. Most of the studies reviewed are of poor quality, so that no logical conclusions can be drawn yet. Most studies on the epigenetic impact of eating disorders have focused exclusively on DNA methylation. It was cross-sectional and centered mainly on females. For example, in primary studies of eating disorders, the global level of DNA methylation was measured and compared with healthy individuals, or DNA methylation was evaluated in selected candidate genes. Anorexia nervosa is a type of eating disorder. An experiment on female blood samples with anorexia nervosa showed hypomethylation of the SLC6A4 gene.[193]Extensive genome methods were also used to study epigenetic changes in EWAS.[194] DNA methylation was examined at the genome level in four groups: 75 women with active anorexia nervosa, 31 women recovered from anorexia nervosa, 41 women without eating disorders (NED), and a control group of 52. Most methylations were found on 58 genes involved in psychiatric status (serotonin receptor activity), immune and metabolic function, and nutrition (fat and glucose metabolism). Methylation levels at 64 sites associated with insulin function, genes regulating glutamate and serotonin activity were discovered. As well, increased methylation at 73 different sites related to inflammatory processes, immunity, olfactory, lipid metabolism, and glucose is associated with increased index of body mass.[109]
Evaluation of potential health effects associated with occupational and environmental exposure to styrene – an update
Published in Journal of Toxicology and Environmental Health, Part B, 2019
M.I. Banton, J.S. Bus, J.J. Collins, E. Delzell, H.-P. Gelbke, J.E. Kester, M.M. Moore, R. Waites, S.S. Sarang
The effect of protein-deficient diet in combination with styrene on neurobehavioral effects was studied in female rats by Khanna, Husain, and Seth (1994). Normal and protein-deficient diet was supplied from the age of 21 days followed by oral exposure at 0 or 250 mg/kg bw/day from postnatal days 36–51. For this dosing period, half of the animals were fed normal diets, and half were fed protein-deficient diets. This study found body weight reduction, an increase in foot shock-induced aggressive behavior and an increase in amphetamine-induced locomotor activity under deficient diet that was aggravated by combined styrene exposure. Levels of norepinephrine, dopamine, and serotonin in the brain were significantly decreased after the combination of styrene exposure and deficient diet in comparison to protein-deficient diet without styrene. A similar pattern was observed for effects on dopamine and serotonin receptor binding in corpus striatum. No effects were noted after styrene treatment under normal diet. The study indicates that protein deficiency during early development is a potential predisposing factor in the expression of neurobehavioral toxicity of styrene. However, the significance of the interaction of styrene with malnutrition for human risk assessment is not clear.
Arsenic, cadmium, and mercury-induced hypertension: mechanisms and epidemiological findings
Published in Journal of Toxicology and Environmental Health, Part B, 2018
Airton da Cunha Martins, Maria Fernanda Hornos Carneiro, Denise Grotto, Joseph A Adeyemi, Fernando Barbosa
In the same vein, As also affects contractile function in vascular smooth muscle (De Lanerolle and Paul 1991). Following phenylephrine-induced contraction, serotonin (5-HT) and/or high concentrations of potassium ions (K+) were measured as well as the mechanisms involved such as mediation by myosin light chain (MLC) phosphorylation and intracellular Ca ions influx. Vascular smooth muscle contraction occurs due to a sudden rise in intracellular free Ca2+ ions, which bind to calmodulin, resulting in a complex of Ca-calmodulin. The complex then activates myosin light chain kinase which further phosphorylates MLC resulting in vasoconstriction (De Lanerolle and Paul 1991). Lee et al. (2005) showed that As3+ enhanced vascular contraction induced by phenylephrine, 5_HT, and high K+ in a concentration-dependent manner. However, a difference regarding the mode of action was considered. Phenylephrine and 5-HT act on the α1-adrenoceptor and the 5-HT2 serotonin receptor, respectively, resulting in increases in intracellular Ca2+ levels, formation of the Ca–calmodulin complex, activation of MLC kinase and phosphorylation of MLC. High concentrations of K+, in turn, are associated with a direct elevation in intracellular Ca2+ concentrations by opening Ca2+ channels due to membrane depolarization. Although Lee et al. (2005) reported the As-induced hypercontraction effect stimulated by phenylephrine as evidenced by MLC phosphorylation, direct Ca2+ measurement also showed that As potentiated vasoconstriction induced by high K+ levels. Therefore, data suggested that, rather than direct increases in Ca2+ levels, Ca2+ sensitization may be a major contributor to the enhanced vasoconstriction induced by As. Further As-enhanced contraction is primarily due to hypercontraction of smooth muscle, since the contraction noted in aortic rings occurred without endothelium (Lee et al. 2005).