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The Pineal Gland and Melatonin
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Jerry Vriend, Nancy A.M. Alexiuk
The mammalian pinealocyte is difficult to classify. Although the pineal gland is attached to the brain, it is not typical neural tissue; nerve cells are not commonly found in the pineal glands of adult mammals. In spite of the apparent endocrine role of the mammalian pineal gland, pinealocytes do not have the appearance of cells that secrete either peptide or steroid hormones. The pinealocyte must be considered a unique derivative of ependymal cells,68 a cell type in its own right. Classifying pinealocytes as paraneurons may, however, add to an understanding of these cells. Synaptophysin and synapsin I, usually considered to be specific for synaptic vesicles of neurons, have been found concentrated in microvesicles in pinealocyte terminals.69
Histology and Pathology of the Human Neuromuscular Junction with a Description of the Clinical Features of the Myasthenic Syndromes
Published in Marc H. De Baets, Hans J.G.H. Oosterhuis, Myasthenia Gravis, 2019
F.G.I. Jennekens, H. Veldman, John Wokke
Synaptic vesicles are formed in the neuron cell body and transported by fast axonal transport to the the motor nerve terminal.21,22 Once arrived in the terminal they need to be translocated to the presynaptic membrane (Figure 5). Proteins in the vesicle wall assist in translocation and in fusion of the vesicles with the plasma membrane. Synapsin, a family of four, homologous, synaptic vesicle specific proteins helps in moving the vesicles along the cytoskeletal system in the nerve terminal towards the “active zones”, the docking areas of the presynaptic membrane. In frogs, the vesicles are accumulated near these active zones but this is not obvious on transmission electronmicrographs of human nerve terminals as the active zones are not easily identified. Close to the active zones, the vesicles become attached to an actin network which in its turn is linked to the plasma membrane by fodrin (brain spectrin). Synaptophysin, the most abundant of the vesicle wall proteins, may participate in forming fusion pores for synaptic vesicle exocytosis (see for review of vesicle wall and active zone proteins references 17 and 23 and Chapter 3).
Gene Targeting Models of Epilepsy: Technical and Analytical Considerations
Published in Steven L. Peterson, Timothy E. Albertson, Neuropharmacology Methods in Epilepsy Research, 2019
The advent of gene targeting technology has produced a dramatic increase in the number of mutant epilepsy models. The first of these, serotonin 5-HT2C receptor null mutant mice, was reported in 1995.11 Subsequently, at least nine additional transgenic mouse epilepsy models have been reported. This cohort of models illustrates the great diversity of genes that are involved in the regulation of neuronal network excitability. Some of the targeted gene products play direct roles in synaptic transmission, such as the 5-HT2C and glutamate GluR-B receptors, the GLT-1 glutamate transporter, and synaptic vesicle proteins, synapsins I and II.12-14 Others play indirect roles in synaptic transmission, such as Ca2+/calmodulin-dependent protein kinase II (CaMKII), a protein kinase that is critical to neuronal signaling,15 the GAD65 isoform of glutamic acid decarboxylase, a GABA synthetic enzyme,16 and nonspecific alkaline phosphatase, which regulates a cofactor required for GABA synthesis.17 In contrast with the above models, other mutations of genes implicated in neuronal excitability are associated with a surprising absence of seizures. Examples include mice lacking the potassium channel Kv 3.118 and the GABA ß3 receptor subunit.19
Investigation of possible associations of the BDNF, SNAP-25 and SYN III genes with the neurocognitive measures: BDNF and SNAP-25 genes might be involved in attention domain, SYN III gene in executive function
Published in Nordic Journal of Psychiatry, 2022
Hilmi Bolat, Gül Ünsel-Bolat, Semiha Özgül, Erhan Parıltay, Akın Tahıllıoğlu, Luis Augusto Rohde, Haluk Akın, Eyüp Sabri Ercan
In the same line with BDNF gene, there are conflicting results about the association of Synaptosomal-Associated Protein 25 (SNAP25) and Synapsin III (SYN III) genes and ADHD diagnosis [8,12–18]. The SNAP25 gene is encoding a protein that is responsible for the release of neurotransmitters by vesicle fusion. Also, the SNAP25 gene was implicated in neuronal growth, differentiation, neurotransmitter release and synaptic plasticity which are underlying processes of attention, memory, learning and other cognitive processes [19]. The major variants studied were rs362987 (intron 4), rs363006 (intron 6), rs3746544 (3′-UTR), and rs1051312 (3′-UTR) [8]. The main effect on ADHD susceptibility was observed especially with the rs3746544 variant [8]. Liu et al. conducted a meta-analysis and found that both rs3746544 and rs1051312 polymorphisms may have possibly higher odds of developing ADHD [20]. Also, there are studies that report SNAP25 gene polymorphisms are associated with adult ADHD diagnosis, not childhood ADHD [21]. Synapsins are neuronal vesicle proteins and SYNIII gene is encoding a protein that is especially responsible for synaptic transmission of dopamine [22].
Abnormal larval neuromuscular junction morphology and physiology in Drosophila prickle isoform mutants with known axonal transport defects and adult seizure behavior
Published in Journal of Neurogenetics, 2022
Atsushi Ueda, Tristan C. D. G. O’Harrow, Xiaomin Xing, Salleh Ehaideb, J. Robert Manak, Chun-Fang Wu
It is evident that the Drosophila larval neuromuscular preparation will remain as a highly relevant model to investigate the complex role of Prickle in neural development and function. It is known that pk mutations confer a spectrum of neurological phenotypes, most likely through interactions with a variety of synaptic proteins. Immunohistochemical and co-immunoprecipitation evidence indicates that mouse PRICKLE1 protein is physically associated with the protein SYNAPSIN I (Paemka et al., 2013), a major synaptic phosphoprotein, and that in the Drosophila larval NMJ transgenic Pk also co-localizes with Synapsin (Paemka et al., 2013). Drosophila Synapsin is known to influence synaptic development, synaptic vesicle formation, and transmitter release (Vasin et al., 2014). It will be important to examine whether interaction between Synapsin and Prickle plays a role in NMJ morphology and physiology. Notably, in addition to epilepsy, a link has been implicated between human PRICKLE mutations and autism (Sowers et al., 2013; Todd & Bassuk, 2018), which may involve disrupted physical association between PRICKLE1 and SYNAPSIN I (Paemka et al., 2013).
Flavanol-rich lychee fruit extract substantially reduces progressive cognitive and molecular deficits in a triple-transgenic animal model of Alzheimer disease
Published in Nutritional Neuroscience, 2021
Xiao Chen, Benhong Xu, Luling Nie, Kaiwu He, Li Zhou, Xinfeng Huang, Peter Spencer, Xifei Yang, Jianjun Liu
Oligonol treatment also modulated the expression of synaptic proteins (DC1I1, dynamin-1, synapsin II and vimentin) in the hippocampi of 3×Tg-AD mice. DC1I1 transports cargos from axon terminals to neuron cell bodies [49]. Dynamin-1 releases intracellular substances from synaptic vesicles [50]. Synapsin II regulates the pool of synaptic vesicles [51]. Vimentin expression is related to synaptic damage [52]. In the present study, both dynamin-1 and synapsin II were reduced in 3×Tg-AD mice and increased by Oligonol treatment, whereas DC1I1 and vimentin were reduced. These findings together with evidence of observed alterations in Aβ and tau suggest synaptic damage, which could explain the associated memory dysfunction displayed by 3×Tg-AD mice [53,54]. In addition, dysfunction of the electron transport chain [55] and UPR [47] could exacerbate the synapse dysfunction. We observed a significant loss of synaptic proteins in 3×Tg-AD mice and the retention of some synaptic proteins with Oligonol treatment (Figure 3). The consistent findings from Western-blot analyses and the proteomics study suggest that Oligonol treatment maintained synaptic integrity and memory function.