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Neuroendocrine Factors
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Catecholamines are stored in terminal boutons within synaptic vesicles; release occurs by exocytosis (120, 139). Synaptic transmission is terminated by a number of factors including: Synaptic concentration dilution by diffusion out of the synapse.Synaptic enzyme catechol-O-methyltransferase (COMT).Reuptake, which is the primary terminator of transmission.
Acid-Sensing Ion Channels and Synaptic Plasticity: A Revisit
Published in Tian-Le Xu, Long-Jun Wu, Nonclassical Ion Channels in the Nervous System, 2021
Ming-Gang Liu, Michael X. Zhu, Tian-Le Xu
Synaptic plasticity is a generic term that applies to short- or long-lasting experience- or activity-dependent changes in the efficacy or connection of synaptic transmission in the brain. It can be classified into both functional and structural aspects of synaptic plasticity. For the former, except for LTP and LTD, it also includes short-term plasticity (like paired-pulse facilitation or depression), depotentiaion86, metaplasticity (plasticity of synaptic plasticity)87, and homeostatic plasticity88 (scaling up or down of the synaptic strength in response to reduction or elevation of synaptic activity). For the latter, dendritic spines may undergo activity-dependent dynamic alterations in shape, size, density, or even composition during various behavioral tasks and/or synaptic stimulations84. To date, most studies have focused on the classical LTP, with much less emphasis placed on other forms of synaptic plasticity, although the possibilities that ASICs are equally important for depotentiaion (or metaplasticity) have not been fully excluded. It would be both necessary and exciting in future studies to test these possibilities.
Neuronal Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Synaptic transmission in mammals usually occurs via chemical neurotransmitters (Figure 4.12). The presynaptic terminal is depolarized by an action potential, which opens voltage-gated calcium channels; calcium ions flow into the presynaptic terminal and cause neurotransmitter vesicles to fuse with the presynaptic membrane. The neurotransmitter is thus released into the synaptic cleft by exocytosis; it diffuses across the synaptic cleft and binds to receptors on the postsynaptic membrane and alters its permeability. The receptors in the postsynaptic membrane may be either ion channels or coupled with G proteins, which activate a second messenger system.
Homocysteine can aggravate depressive like behaviors in a middle cerebral artery occlusion/reperfusion rat model: a possible role for NMDARs-mediated synaptic alterations
Published in Nutritional Neuroscience, 2023
Mengying Wang, Xiaoshan Liang, Qiang Zhang, Suhui Luo, Huan Liu, Xuan Wang, Na Sai, Xumei Zhang
Synaptic transmission and plasticity are known to be susceptible to various environmental factors and, accordingly, synaptic dysfunction and degeneration occur early in the pathogenesis of several different neurological disorders including stroke, depression and cognitive impairment [41, 42]. Several findings suggest that long-term exposure to HCY induced alterations in spatial learning, hippocampal signaling and synaptic plasticity [43, 44]. In this study, HCY treatment markedly reduced the expressions of synapse-related proteins and resulted in a significant decrease in the number of synapses and postsynaptic density in the hippocampus from the PSD rats. Given the roles for HCY in the pathogenesis of neurological disorders, impaired hippocampus plasticity and synaptic transmission may be at the center of HCY' s contribution to these nervous system diseases. The nervous system may be particularly sensitive to HCY as it may trigger neuronal damage via destroying synaptic structure and function.
Combination of tea polyphenols and proanthocyanidins prevents menopause-related memory decline in rats via increased hippocampal synaptic plasticity by inhibiting p38 MAPK and TNF-α pathway
Published in Nutritional Neuroscience, 2022
Qian Yang, Yusen Zhang, Luping Zhang, Xuemin Li, Ruirui Dong, Chenmeng Song, Le Cheng, Mengqian Shi, Haifeng Zhao
Dendritic spines are the major sites of excitatory synaptic input, the number of synapses is closely related to the transmission efficiency and the transmission efficiency of nerve impulses [40]. In the model group, decreased density of dendritic spines and decreased number of excitatory synapses impaired the efficiency of nerve conduction. Therefore, we further observed the ultrastructure of synapses by transmission electron microscope. Structural plasticity of synapses is the basis of functional plasticity, mainly manifested as the size of presynaptic and postsynaptic contact area, the number of active areas in the synaptic contact area, the change of synaptic gap (affecting synaptic transmission efficiency) [41]. Classical parameters of synaptic structure include synapse interface curvature, synapse gap width, postsynaptic density (PSD) thickness and numerical density per unit volume (Nv) [42]. Narrow synaptic cleft is advantageous to the pre-synaptic membrane release of neurotransmitters, larger interface curvature can reduce the neurotransmitters into the surrounding interstitial diffusion ensure the neurotransmitter release further to reach the target, improve the transfer function.
Recent advances in electrochemical and optical sensing of the organophosphate chlorpyrifos: a review
Published in Critical Reviews in Toxicology, 2022
Athira Sradha S, Louis George, Keerthana P, Anitha Varghese
It has been classified as an acetylcholinesterase (AChE) inhibitor and works by binding and inhibiting the AChE enzyme in insects and mammals. AChE, is a cholinergic enzyme that is found in the mammalian nervous system, which hydrolyzes acetylcholine into acetate and choline. Acetylcholine is a key neurotransmitter for synaptic transmission (McHardy et al. 2017). The carbonyl carbon of the molecule undergoes nucleophilic attack followed by acylation of the active site of the AChE enzyme to produce choline. Upon hydrolysis of the acylated enzyme, the esterasic site is restored. Organophosphates (OPs) bind to AChE and permanently inactivate the enzyme resulting in an enzyme-phosphorylation complex that is highly stable (English and Webster 2012). On photolysis, aerobic metabolism, or chlorination, CP oxidizes to a more toxic chlorpyrifos oxon (CPO) (Figure 3(B)) which also inhibits AChE resulting in the accumulation of acetylcholine. This is associated with a condition of cholinergic hyperstimulation which produces neurotoxic effects in insects and non-target organisms (Prueitt et al. 2011). Figure 2 explains the mechanism for the formation of AChE and Figure 3 shows the chemical structure of the different forms of chlorpyrifos.