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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
The next series of experiments was performed to link the postsynaptic modifications induced by Pb2+ with presynaptic mechanisms regulated by BDNF-TrkB signaling (Figure 4.17). BDNF released from dendritic spines activates TrkB downstream pathways, including MAPK PI3K, and PLCγ.411 It is thought that mBDNF modulates synaptic neurotransmission by presynaptic TrkB activation,412 and it has been shown that BDNF-induced neurotransmitter release is partially blocked by TrkB inactivation.413,414 Their data reveal significant reductions in tTrkB protein expression by Pb2+ as well as reductions in TrkB autophosphorylation at Y816. Phosphorylation of TrkB at Y816 has been directly linked with PLCγ activation and mobilization of intracellular Ca2+, release of presynaptic BDNF and glutamate,412,413 and activation of CaMKII-CREB.414,415 Furthermore, TrkB coupling to PLCγ signaling via Y816 phosphorylation is essential for long-term potentiation (LTP) in the hippocampus416 and associative learning.417 These results provide a putative mechanism by which a Pb2+-induced impairment in the coupling of TrkB activation with downstream Ca2+ and CaMKII signaling can inhibit LTP and learning. Relevant to this observation, animals exposed to Pb2 during development express deficits in hippocampal LTP and spatial learning as young adults.418 These new findings provide important mechanistic insights to help explain Pb2+ effects on synaptic plasticity and learning.
Effects of mild running on substantia nigra during early neurodegeneration
Published in Journal of Sports Sciences, 2018
Michael F. Almeida, Carolliny M. Silva, Rodrigo S. Chaves, Nathan C. R. Lima, Renato S. Almeida, Karla P. Melo, Marilene Demasi, Tiago Fernandes, Edilamar M. Oliveira, Luis E. S. Netto, Sandra M. Cardoso, Merari F. R. Ferrari
The present data corroborate previous studies that associate decrease in TrkB receptors during neurodegeneration, which is associated with the possible feedback effect of increase in motor proteins of these receptors. However, results presented herein demonstrated that proteins associated to BDNF system, such as TrkB receptor and proteins related to anterograde trafficking of TrkB receptor, seem not to be involved with the cellular protection of moderate physical activity during early neurodegeneration, as well established for late PD animal models where neuron loss is present (Real et al., 2013; Wu et al., 2011b).