Histology and Pathology of the Human Neuromuscular Junction with a Description of the Clinical Features of the Myasthenic Syndromes
Marc H. De Baets, Hans J.G.H. Oosterhuis in Myasthenia Gravis, 2019
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).
The Exercise Effect on Mental Health in Older Adults
Henning Budde, Mirko Wegner in The Exercise Effect on Mental Health, 2018
Various animal studies identified several mechanisms whereby PA and exercise may facilitate neuroplasticity. Exercise seems to increase the expression of synaptic plasticity genes, gene products (synapsin, synaptophysin), and various neuroplasticity-related transcription factors (Berchtold, Castello, & Cotman 2010; Shen, Tong, Balazs, & Cotman 2001). Furthermore, hippocampal dendritic length and dendritic spine complexity can be enhanced through exercise (Eadie, Redila, & Christie 2005; Redila & Christie 2006). Additional research provides evidence that exercise induces neurogenesis within the hippocampal dentate gyrus (van Praag, Kempermann, & Gage 1999; Eadie et al. 2005; Redila & Christie 2006; Fabel et al. 2003) even in older ages (van Praag, Shubert, Zhao, & Gage 2005; Kronenberg et al. 2006).
Exercise, neurotransmission and neurotrophic factors
Romain Meeusen, Sabine Schaefer, Phillip Tomporowski, Richard Bailey in Physical Activity and Educational Achievement, 2017
As stated before, both aerobic (endurance) exercise and strength training will positively influence cognitive performance. However, strength training does not seem to influence BDNF, therefore there must be another mechanism involved. We evaluated the effects of resistance training on spatial memory and the signalling pathways of BDNF and insulin-like growth factor 1 (IGF-1), comparing these effects with those of aerobic exercise (Cassilhas et al., 2012). Adult male Wistar rats underwent 8 weeks of aerobic training on a treadmill (AERO group) or resistance training on a vertical ladder (RES group). After the training period, both AERO and RES groups showed improved learning and spatial memory in a similar manner. However, both groups presented distinct signalling pathways. Although the AERO group showed increased levels of IGF-1, BDNF, tyrosine receptor kinase B and calcium/calmodulin-dependent kinase II in the hippocampus, the RES group showed an induction of peripheral and hippocampal IGF-1 with concomitant activation of receptor for IGF-1 (IGF-1R) and AKT in the hippocampus. These distinct pathways culminated in an increase of synapsin 1 and synaptophysin expression in both groups. These findings demonstrated that both aerobic and resistance exercise can employ divergent molecular mechanisms but achieve similar results on learning and spatial memory (Cassilhas et al., 2012).
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.
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).
RLIPostC protects against cerebral ischemia through improved synaptogenesis in rats
Published in Brain Injury, 2018
Yingli Wang, Zhaohui Zhang, Lei Zhang, Haoran Yang, Zhiqiang Shen
Synapsin 1 (Syn1) is a member of the synapsin gene family, which plays an important role in the regulation of synaptogenesis. Here, we detected the effects of RLIPostC treatment on the expression of Syn1 at day 14 after MCAO by western blotting. The results showed that RLIPostC treatment significantly upregulated the expression of Syn1 (p < 0.05, Figure 4(a)) compared to the control group. Interestingly, although there was no statistical difference, the expression of Syn1 in the RLIPostC treatment group was higher than that in the sham group (p = 0.32).