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Ayahuasca
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Wild Plants, 2020
Raquel Consul, Flávia Lucas, Maria Graça Campos
As MAO is responsible for endogenous neurotransmitter degradation, its inhibition alters, albeit indirectly, the homeostasis of the dopaminergic, adrenergic, and serotonergic systems, which is reflected in greater dopamine circulation, for example (Alsuntangled 2017). In addition to other less-studied mechanisms, the dopamine transport inhibition at high concentrations, specific inhibition of tyrosine-1A-phosphorylation regulatory kinase, as well as affinity for the imidazoline binding site contributes to this. Harmine, by way of example, also acts in the regulation of the excitatory amino acid transporter-2, as a primary mechanism of synaptic glutamate inactivation, as well as causing an inverse agonist effect at the benzodiazepine binding site on the GABAA (γ-aminobutiric acid) receptor (Hamill et al. 2018).
Improved Management of Autism Spectrum Disorder (ASD) by Micronutrients
Published in Kedar N. Prasad, Micronutrients in Health and Disease, 2019
In the autopsied mainly cerebellum samples from patients with ASD, the mRNA levels of several genes, including excitatory amino acid transporter 1 and glutamate receptor AMPA 1 were increased.83 In the autopsied brain samples, the levels of Fragile X mental retardation protein (FMRP) and GABA (A) receptor beta 3 (GABARbeta3) decreased in the vermis of adult patients with ASD, whereas the levels of metabotropic glutamate receptor 5 (mGluR5) increased in the vermis of children with ASD.84
Ciguatera: A Treating Physician's Perspective on a Global Illness
Published in Dongyou Liu, Handbook of Foodborne Diseases, 2018
Ritchie C. Shoemaker, James C. Ryan
Adding to the fascinating discovery of differential gene activation seen after ciguatoxin exposure, the finding from Zhang (94) showed that intracerebroventricular administration of ciguatoxin in rats increased levels of glial fibrillary acidic protein (GFAP) expression in reactive astrocytes. Additional gene activation included gap junction protein connexin 43 and upregulation of excitatory amino acid transporter 2. GFAP suppresses regrowth of neurons after injury; it has been a focus of mine regarding the absence of central nervous system healing in CIRS-WDB. Though we cannot assay GFAP in brain, and GFAP is not found in peripheral blood, we are beginning to look at cerebrospinal fluid, since we have shown that use of high-dose vasoactive intestinal polypeptide (VIP) restores gray matter nuclear atrophy (95). It remains plausible to look further at genomic effects induced by ciguatoxin affecting brain volumes.
Glutamatergic dysregulation in mood disorders: opportunities for the discovery of novel drug targets
Published in Expert Opinion on Therapeutic Targets, 2020
Panek Małgorzata, Kawalec Paweł, Malinowska Lipień Iwona, Tomasz Brzostek, Pilc Andrzej
The glutamatergic system is a major brain-stimulating system, with glutamate (Glu) as the primary neurotransmitter. Glutamatergic projections connect a number of brain structures such as the efferent routes from the cortex to the thalamus as well as to the nucleus accumbens, septum, and amygdala. Glu reaches synaptic vesicles via the vesicular glutamate transporter and is secreted from presynaptic endings in response to neuronal depolarization. This is followed by glutamate reuptake into cells (such as glial, brain and neuronal cells) via the excitatory amino-acid transporter (EAAT). The conversion of Glu to glutamine occurs in glial cells, by a reaction catalyzed by the enzyme glutamine synthetase, which occurs only in these cells. Glutamine is released to the extracellular space, from where it is absorbed back to glutamatergic neurons. Glutamine is again converted into glutamate by the glutaminase enzyme [13].
Discovery of differentially expressed genes in the intestines of Pelteobagrus vachellii within a light/dark cycle
Published in Chronobiology International, 2020
Chuanjie Qin, Jiaxian Sun, Jun Wang, Yongwang Han, He Yang, Qingchao Shi, Yunyun Lv, Peng Hu
Moreover, a diurnal rhythmicity was noted for peptide absorption, for example, in nocturnal animals, the L-histidine absorption peak occurs during the dark phase(Furuya and Yugari 1974), which is coincident with higher expression levels of peptide transporter HPEPT1 (PEPT1) in the the dark compared with that in the light (Pan et al. 2002). In this study, b(0,+)-type amino acid transporter 1, sodium-coupled neutral amino acid transporter B, sodium-dependent neutral amino acid transporter 3, and excitatory amino acid transporter 1, all displayed upregulation at night, which contrasted with that of low affinity cationic amino acid transporter 2, a large neutral amino acids transporter. Excitatory amino acid transporter 1 is a sodium-dependent, high-affinity amino acid transporter that mediates the uptake of L-glutamate, L-aspartate, and D-aspartate (Arriza et al. 1994). The high-affinity transport of large neutral amino acids (e.g., phenylalanine, tyrosine, leucine, arginine, and tryptophan) is affected by sodium-independent, large neutral amino acids transporters. The peak time of mRNA expression was different for digestive enzymes and amino acid transporters within a light/dark cycle, which might suggest that the digestion and absorption of different amino acids was occurred at different times. Similarly, Senegalese sole (Solea senegalensis) showed their highest post-larval protein retention capacities when fed at nighttime (Marinho et al. 2014).
Clinical phenotype and genetic risk factors for bipolar disorder with binge eating: an update
Published in Expert Review of Neurotherapeutics, 2019
Alfredo B. Cuellar-Barboza, Stacey J. Winham, Joanna M. Biernacka, Mark A. Frye, Susan L. McElroy
Environmental factors can be explored with epigenetic studies, which quantify genomic changes in response to external influence. To our knowledge, only one study has evaluated the epigenetic effect of BE in BD. Jia and colleagues [153] compared the methylation of SLC1A2 promoter between BD patients with variable environmental influences of addiction (i.e. alcohol, nicotine, or food defined as binge eating) and healthy controls. Coded by SLC1A2, the excitatory amino acid transporter 2 (EAAT2) is the main transporter removing glutamate from the synapse, and its activity has been shown to be altered in BD. In this investigation, the authors found the SLC1A2 promoter region to be hypermethylated in BD alone, but it was hypomethylated in BD with nicotine addiction (p = 0.0009) and BE behavior (p = 0.0002). This finding suggests that certain behaviors such as BE may produce epigenetic changes that are either compensatory to other epigenetic modifications or preserve aberrant behaviors [153]. However, the methodology of this study had important limitations, including those inherent to its cross-sectional design, small sample size, and lack of independent replication. Further steps required to expand upon these findings would include conducting studies with longitudinal designs, replication in brain tissue, more comprehensive exploration of the genome, and establishing a strictly refined phenotype to avoid potential confounders.