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Homeostasis of Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
The SNARE complex is formed by members of the synaptosomal-associated protein 25 (SNAP-25), vesicle-associated membrane protein (VAMP) and members of the syntaxins family. Interactions between these proteins create a four-helix bundle, formed by two helices of SNAP-25, one vesicular-transmembrane VAMP and one presynaptic plasma membrane syntaxin that brings together the vesicular and plasmatic membranes. Other proteins that interact with the SNARE complex include Munc-18, complexin, synaptophysin, and synaptotagmin [77]. In addition, synaptotagmin serves as a calcium sensor and regulates the SNARE zipping. The SM proteins are evolutionary conserved cytosolic proteins that serve as essential partners for SNARE proteins in fusion. Among these is Munc 18, which primarily interacts with syntaxin-1 and whose function is tightly regulated by calcium.
Pharmacotherapy of Neurochemical Imbalances
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rupali Patil, Aman Upaganlawar, Suvarna Ingale
Other molecule which is able to bind Ca2+ is the phosphatase calcineurin that is a serine/threonine phosphatase. Occupation of the calcium-binding site makes a structural change that exposes a Ca2+-CaM binding site. Once Ca2+-CaM binds to a subunit, it becomes active, dephosphorylation a number of intracellular targets. Exocytosis process of neurotransmitter release from synaptic vesicles is known to be mediated via Synaptotagmin present in all neurons (Claudia and Fabiola, 2014).
Botulinum toxins: Pharmacology, immunology, and current developments
Published in Anthony V. Benedetto, Botulinum Toxins in Clinical Aesthetic Practice, 2017
Synaptotagmins I and II are protein receptors for BoNT types B and G.33,34 Synaptotagmins are localized to synaptic vesicle membranes where they sense calcium and trigger vesicle fusion.35 Binding of types B and G to these proteins leads to their internalization into neurons.34,36
Vortioxetine in management of major depressive disorder – a favorable alternative for elderly patients?
Published in Expert Opinion on Pharmacotherapy, 2021
One of the significant neurological disorders present in the elderly population is AD. Studies in patients and animal models revealed that vortioxetine might help manage the symptoms of this neurodegenerative disease. In a randomized study, 108 patients with AD receive either vortioxetine or another common antidepressant – escitalopram, paroxetine, bupropion, venlafaxine, or sertraline [49]. After 12 months of treatment, vortioxetine-treated subjects significantly improved their performance in Mini-Mental State Examination, Attentive Matrices, and Raven Colored Progressive Matrices. Such effects were not observed in the control group, which received alternative treatment. The studies on the animal model may provide some explanation on the mechanism of this activity. The research was conducted on the transgenic mouse model (5xFAD) [50]. Although vortioxetine did not delay the formation of β-amyloid plaques, increased expression of postsynaptic density protein 95, synaptophysin, and synaptotagmin-1 suggests that this drug may have a beneficial effect on synaptic function. Also, vortioxetine reversed the reduction in anxiety-type behavior.
Marinoid J, a phenylglycoside from Avicennia marina fruit, ameliorates cognitive impairment in rat vascular dementia: a quantitative iTRAQ proteomic study
Published in Pharmaceutical Biology, 2020
Xiang-xi Yi, Jia-yi Li, Zhen-zhou Tang, Shu Jiang, Yong-hong Liu, Jia-gang Deng, Cheng-hai Gao
Signal transmission at the neuromuscular junction is mediated via the release of acetylcholine from synaptic vesicles. This process is rendered calcium-sensitive by members of the Synaptotagmin family, which also has roles in vesicle priming and in reducing spontaneous neurotransmitter release (Lee et al. 2008). SYT2 is the major isoform expressed at the neuromuscular junction, and previous studies have shown that Syt2 knockout mice show markedly reduced calcium-evoked neurotransmitter release (Pang et al. 2006). A previous study (Whittaker et al. 2015) found that Syt2 mutations cause a novel and potentially treatable complex presynaptic congenital myasthenic syndrome characterized by motor neuropathy inducing lower-limb wasting and foot deformities. A recent study (Bereczki et al. 2018) used in-depth proteomics to compare 32 post-mortem human brains in the prefrontal cortex of prospective AD patients, PD patients with dementia, dementia patients with Lewy bodies, and older adults without dementia. They found a significant loss of SYT2, which implicates that it could be a synaptic marker of cognitive decline in neurodegenerative diseases. Our present study showed that abnormal expression of SYT2 may be related to the occurrence of VD, and PGs may decrease the expression of SYT2 in VD rats, thereby alleviating the symptoms of VD rats.