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Genetic and environmental determinants of adolescent alcohol use
Published in Ilana B. Crome, Richard Williams, Roger Bloor, Xenofon Sgouros, Substance Misuse and Young People, 2019
Toni-Kim Clarke, Richard C. Crist
Targeted studies of single variants or candidate genes have been somewhat more successful than GWAS in identifying genotypic associations with adolescent alcohol use. Altered regulation of monoamine neurotransmitters, such as serotonin and dopamine, is a common factor in many psychiatric diseases, including alcoholism (Yoshimoto et al., 1992). Polymorphisms in the genes regulating neurotransmitter release and downstream signalling may affect susceptibility to alcohol use disorders. The serotonin transporter, 5-HTT, is responsible for the uptake of serotonin from the synaptic cleft. A polymorphic repeat region known as 5-HTTLPR occurs in the 5-HTT promoter and is primarily classified into long and short alleles. Nilsson et al. (2006) found that the genotype at 5-HTTLPR was associated with alcohol consumption during adolescence, while other research identified an association between the polymorphism and early alcohol use (Kaufman et al., 2007). Both studies found that teenagers carrying one long and one short allele were at the highest risk. In a subsequent study in the Netherlands, the short allele of 5-HTTLPR was associated with the rate of increase in alcohol consumption over time by adolescents (van der Zwaluw et al., 2010b).
The cell
Published in Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella, Essentials of Human Physiology and Pathophysiology for Pharmacy and Allied Health, 2019
Laurie K. McCorry, Martin M. Zdanowicz, Cynthia Y. Gonnella
The third mechanism by which drugs may alter synaptic activity involves changes in neurotransmitter re-uptake or degradation. Very well-known examples of drugs in this category are Prozac® (fluoxetine) and the more recently prescribed Cymbalta® (duloxetine) and Wellbutrin® (bupropion), which are used to treat depression. While the complete etiology is unknown, it is widely accepted that depression involves a deficiency of monoamine neurotransmitters (e.g., norepinephrine and serotonin) in the CNS. Prozac, a selective serotonin re-uptake inhibitor, prevents the removal of serotonin from the synaptic cleft. Cymbalta prevents the re-uptake of both serotonin and norepinephrine, whereas Wellbutrin prevents the re-uptake of dopamine and norepinephrine. Therefore, the concentration and activity of these neurotransmitters in the brain are enhanced and the symptoms of depression are relieved.
Resilience and burnout
Published in Anna-leila Williams, Integrating Health Humanities, Social Science, and Clinical Care, 2018
Concurrent with activation of the hypothalamic-pituitary-adrenal axis, stress leads to activation of the sympathetic nervous system and inhibition of the parasympathetic nervous system. Consequently, monoamine neurotransmitters, norepinephrine and dopamine are released in response to stress which facilitates encoding emotionally charged memories at the amygdala. Hypersecretion of norepinephrine is associated with anxiety and post-traumatic stress disorder. Another monoamine neurotransmitter, serotonin, has not had its mode of physiologic influence precisely delineated as of yet. That said, it is widely accepted that serotonin metabolites modulate the amygdala and prefrontal cortex to mitigate physiologic responses to stress. Serotonin effects on the body are known to include regulation of anxiety, mood, aggression, and impulse control, and therefore are presumed to contribute to resilience (Krystal & Neumeister, 2009).
Homocysteine can aggravate depressive like behaviors in a middle cerebral artery occlusion/reperfusion rat model: a possible role for NMDARs-mediated synaptic alterations
Published in Nutritional Neuroscience, 2023
Mengying Wang, Xiaoshan Liang, Qiang Zhang, Suhui Luo, Huan Liu, Xuan Wang, Na Sai, Xumei Zhang
It has been reported that the levels of monoamine neurotransmitters, especially DA, 5-HT, and NE are related to the neurobiological mechanism of depression [26]. To confirm whether these depressive-related neurotransmitters were involved in the depression process induced by HCY in the MCAO rats, the levels of NE, DA and 5-HT in plasm were analyzed by HPLC. The results demonstrated that the concentrations of 5-HT (3.49 ± 0.44 ng/mL), DA (28.40 ± 4.00 μg/L) and NE (8.44 ± 1.59 μg/L) were significantly reduced in the MCAO group in comparison with the SHAM group (7.45 ± 1.50 ng/mL, 63.60 ± 8.71 μg/L, 16.22 ± 5.77 μg/L; P < 0.05). Further, HCY treatment significantly depleted the monoamine neurotransmitters (5-HT: 9.14 ± 7.84 ng/mL, DA: 10.20 ± 6.22 μg/L, NE: 2.364 ± 0.57 μg/L) when compared to those of the MCAO rats (P < 0.001, P < 0.001, P = 0.013; Figure 2(e–f)). These data revealed that HCY might deteriorate depressive-like behaviors in MCAO rats.
Lycopene and Chrysin through Mitigation of Neuroinflammation and Oxidative Stress Exerted Antidepressant Effects in Clonidine-Induced Depression-like Behavior in Rats
Published in Journal of Dietary Supplements, 2023
Ekram Nemr Abd Al Haleem, Hebatalla I. Ahmed, Reem N. El-Naga
In addition to the behavioral tests, the tissue levels of monoamines in rats’ hippocampus were assessed in the different treatment groups. Monoamine neurotransmitters (e.g. dopamine, norepinephrine (NE), and 5-HT) are eminent in the central nervous system and are thought to play a significant role in the pathophysiology of depression (40). Thus, the biogenic amine hypothesis or monoamine theory suggests that the brain’s reduced monoaminergic activity characterizes depression. In this context, all the commercially available antidepressants work via countless mechanisms to surge synaptic concentrations of monoamines (41). The current results showed that the monoamine levels in the brain were markedly elevated in the clonidine group. Nevertheless, lycopene or chrysin significantly lessened this effect. These findings confirm the involvement of the serotoninergic and adrenergic systems in the anti-depressant-like effect of lycopene and chrysin.
A case report of infantile parkinsonism-dystonia-2 caused by homozygous mutation in the SLC18A2 gene
Published in International Journal of Neuroscience, 2023
Hongyin Zhai, Yaofeng Zheng, Yiduo He, Yong Zhang, Zhikuan Guo, Wenzhe Cui, Li Sun
The monoamine neurotransmitter disorders are neurometabolic syndromes caused by disturbances in the synthesis, transport and metabolism of the biogenic amines (the catecholamines dopamine, norepinephrine and epinephrine; serotonin), which are increasingly recognized as an expanding group of inherited neurometabolic syndromes [1]. SLC18A2 gene is located on chromosome 10q25 and mainly encodes vesicular monoamine transporter 2 (VMAT2). The membrane protein VMAT2 plays a key role in the accumulation and regulation of the release of dopamine and other monoamines from neuronal cytoplasm into synaptic vesicles [2–4]. Brain dopamine-serotonin vesicular transport disease, a complex motor disorder with severe developmental delays that begins in infancy and is caused by mutations in the SLC18A2 gene, has been reported in three families in different countries [5–7]. The current report on a fourth family highlights that paternal uniparental disomy (UPD)-induced homozygous missense mutations in the SLC18A2 gene are associated with clinically recognized phenotypes, such as static tremor and dystonia, that respond to direct treatment with the dopamine receptor agonist prampexole.