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Inorganic Chemical Pollutants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Studies by Jovanovic et al.392,419 have shown that glutamate and gamma-aminobutyric acid (GABA) release are linked to presynaptic BDNF-TrkB signaling via MAPK phosphorylation of Synapsis I at sites 4/5 (serine 62/67). Synapsin I is a phosphoprotein that is essential for synaptic vesicle trafficking and in the phosphorylated state, it releases vesicles bound to act in filaments allowing their movement from the reserve pool to the RRP (docked vesicle).420 Their data revealed that Pb2+ exposure reduces Synapsin I phosphorylation at serine 62/67 with no change in total Synapsin I protein levels. This novel finding provides a potential explanation to their previous observation400 that Pb 2+ exposure specifically decreases a pool of vesicles with fast-releasing kinetics, which are most likely representative of the RRP (docked vesicles). They are currently performing experiments to determine the number of vesicles in the reserve and RRP (docked vesicles) using electron microscopy in order to test this novel finding. Synapsin I phosphorylation at serine 62/67 modulates vesicle movement from the reserve pool to the RRP in a Ca2+-independent manner, affecting both glutamatergic and GABAergic transmitter release.392,419 These observations are consistent with and support their working model that the effects of Pb2+ on vesicular release are due to presynaptic changes independent of Pb2+ effects on calcium-sensitive proteins or VGCCs and can account for Pb2+ effects on both glutamatergic and GABAergic transmission.400
Applications in Biology
Published in Gabriel A. Wainer, Discrete-Event Modeling and Simulation, 2017
Synapsin is a neuron-specific phosphoprotein that binds to small synaptic vesicles and actin filaments in a phosphorylation-dependent pattern [1]. Microscopic models have demonstrated that synapsin inhibits neurotransmitter release either by forming a cage around synaptic vesicles (cage model) or by anchoring them to the F-actin cytoskeleton of the nerve terminal (cross-linking model) [2].
Learning, memory deficits, and impaired neuronal maturation attributed to acrylamide
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Seulah Lee, Hee Ra Park, Joo Yeon Lee, Jung-Hyun Cho, Hye Min Song, Ah Hyun Kim, Wonjong Lee, Yujeong Lee, Seung-Cheol Chang, Hyung Sik Kim, Jaewon Lee
The present investigation demonstrated that low-dose ACR at 2, 20 or 200 μg/kg administered p.o. for 4 weeks did not markedly alter numbers of proliferating or surviving neural stem cells in hippocampi. However MWM latencies were significantly higher in the 200 μg/kg group, and duration times and cross-over frequencies to find the platform during probe trial were diminished in the 200 μg/kg group, suggesting learning and memory impairments. Since learning and memory are influenced by neural plasticity as well as hippocampal neurogenesis (Del Olmo et al. 2006; VanGuilder et al. 2011), ACR-mediated memory impairments might be associated with changes in brain plasticity, which might be remodeled by external stimulation or learning (Sailor, Schinder, and Lledo 2017; Zhao, Deng, and Gage 2008). In fact, Zhang et al. (2017a) reported that number of synapses and protein levels of synapsin were reduced in the cerebral cortices and cerebella of rats exposed to ACR.