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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.
Synapses
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
It is convenient to distinguish between short-term synaptic plasticity, generally lasting for up to a few minutes, and long-term plasticity, lasting from minutes to hours and even longer if synaptic growth is included. The following should be noted concerning synaptic plasticity: Both short-term and long-term synaptic plasticity can be an enhancement or a depression of synaptic activity.Several processes, and not a single process, are involved in synaptic plasticity, the time courses of these processes, and their relative contributions depending on the particular synapses.The underlying molecular mechanisms of synaptic plasticity may differ in detail between various parts of the brain, but some general principles apply in almost all cases.As will become clear from the following discussion, short-term plasticity is mainly presynaptic, whereas long-term plasticity is mainly postsynaptic.Whereas long-term synaptic plasticity is involved in learning and memory, short-term plasticity affects the encoding of neuronal responses (Chapter 7).
Advances in Understanding the Mechanisms Underlying Synaptic Plasticity
Published in Avital Schurr, Benjamin M. Rigor, BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Timothy J. Teyler, Idil Cavus, Chris Coussens, Pascal DiScenna, Lawrence Grover, Yi-Ping Lee, Zeb Little
Synaptic plasticity refers to an experience-dependent alteration in synaptic strength (or efficacy). Increases (potentiation) and decreases (depression) in synaptic strength are both considered expressions of synaptic plasticity. It is widely assumed that the pattern of activity in a neural network represents information storage in the brain. If correct, then both strengthening and weakening of particular synapses will contribute to network pattern formation, just as excitation and inhibition both contribute to the establishment of sensory representations in primary neocortex. It is thus widely believed that synaptic plasticity within a neural network is responsible for the alterations in brain function responsible for behavioral learning and memory. In this context, the alteration in individual synapses within the active network represents learning and the persistence of that alteration represents memory.
Investigation of the mechanism of tanshinone IIA to improve cognitive function via synaptic plasticity in epileptic rats
Published in Pharmaceutical Biology, 2023
Chen Jia, Rui Zhang, Liming Wei, Jiao Xie, Suqin Zhou, Wen Yin, Xi Hua, Nan Xiao, Meile Ma, Haisheng Jiao
Synaptic plasticity refers to neurons’ ability to alter synaptic connectivity over time (Shefa et al. 2018; Yepes 2020). The loss of synaptic connections in the hippocampus has been linked to the cognitive disorder in epilepsy, suggesting a vital role in its pathogenesis (Jiang et al. 2015; Tang et al. 2017). The dentate gyrus exhibits aberrant synaptic plasticity associated with MFS in chronic human epilepsy and epileptic animal model (Scharfman et al. 2003; Mello and Longo 2009; Twible et al. 2021). Epilepsy may cause an extensive neuronal loss in the hippocampus (Schoene-Bake et al. 2014; Zhao et al. 2020), followed by neuronal network remodelling characterized by severe MFS and granular cell neurogenesis (Lynch and Sutula 2000; Williams et al. 2002; Sloviter et al. 2006). Numerous researchers believe that the death of hippocampal neurons is a crucial factor in the onset of MFS (Sutula and Dudek 2007). This research demonstrated no apparent structural damage in the hippocampal CA3 regions in any tanshinone IIA treatment group, especially in the TS IIA-M and TS IIA-H groups. In contrast, the VPA and model groups showed obvious abnormal MFS, ultrastructural disorder and vacuolar degeneration. The disorganized ultrastructure and blurred tissue morphology of the CA3 area were improved after tanshinone IIA treatment. Tanshinone IIA administration may assist preserve the normal synaptic connection between neurons and alleviate the ultrastructural abnormality and vacuolar degeneration of the hippocampus CA3 region induced by epilepsy.
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 plasticity specifically refers to the activity-dependent modification of the strength or efficacy of synaptic transmission at pre-existing synapses [9]. It is increasingly recognized that synaptic plasticity plays a critical role in functional recovery, such as learning and memory after stroke [10]. The absence of synaptic changes potentially involved in recovery has a negative influence on the final outcome of post-stroke individuals. Additionally, previous studies using an HCY injection model found that HCY changed hippocampus plasticity and synaptic transmission resulting in learning and memory deficits [11–13]. Since depression has been linked to failure in synaptic plasticity originating from environmental and/or genetic risk factors, it is likely that synaptic plasticity may be responsible for HCY-associated depressive symptoms after cerebral ischemic damage.
Deep TMS H7 Coil: Features, Applications & Future
Published in Expert Review of Medical Devices, 2021
Tal Harmelech, Yiftach Roth, Aron Tendler
The goal of rotational field TMS (rfTMS), a newly developed method, is to reduce TMS’s sensitivity to coil orientation with respect to neurons. The principle of the method is to superimpose the field of two orthogonally positioned TMS coils and stagger the two pulses with a 90° (one-fourth cycle) phase delay, thereby producing a circular polarization (i.e. rotating electric field vector). This potentially results in stimulation of a larger portion of the neuronal population in a specific brain region. A recent study compared the effects of rfTMS and unidirectional (conventional) TMS (udTMS) in the hand and foot motor cortices and found that, for comparable induced electric field amplitude, rfTMS induced significantly lower resting motor threshold and higher motor evoked potentials than those induced by udTMS [73]. In other words, rfTMS induces stronger physiological effects in targeted brain regions at significantly lower intensities. With repeated applications, this has the potential for more effective changes in neuronal excitability and synaptic plasticity, and hence enhanced clinical impact in various brain disorders.