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Introduction to botulinum toxin
Published in Michael Parker, Charlie James, Fundamentals for Cosmetic Practice, 2022
The axon is a long tubular structure which extends out of the cell body. The point of attachment to the cell body is known as the axon hillock, and it is at this point where an action potential is usually generated, a change in the polarisation of a neuron to allow propagation of a signal. The axon is surrounded by a myelin sheath which serves to insulate the axon and decrease the loss of electrical signal, similar to electrical cabling in your home. Neuronal impulses do not travel through the axon but skip along the outside of the myelin sheath between areas known as nodes of Ranvier. At the end of the axon is the axon terminal, a specialised region of finger-like projections which are in close proximity with but not touching another nerve or effector cells (such as muscle). See Figure 8.1. The point at which a neuron interacts with another cell is known as a synapse. A synapse is a gap between axon terminals and the next cell, for example a dendrite of another neuron. A synapse is broken down into the presynaptic terminal of the cell conducting an electrical signal and a postsynaptic terminal, which is the region which receives said signal. There are two main types of synapse: electrical and chemical (Figure 8.2).
Nanotechnology in Stem Cell Regenerative Therapy and Its Applications
Published in Harishkumar Madhyastha, Durgesh Nandini Chauhan, Nanopharmaceuticals in Regenerative Medicine, 2022
The characterisation of synaptic and neuronal loss across the brain with impairment in memory and cognition leading to dementia is Alzheimer’s disease. Acetylcholinesterase inhibitors are used to treat AD, which enhances cholinergic function and partially alleviates the symptoms. The competency of the stem cells in delivering the factors will modify the disease stages. Nerve growth factor (NGF) has resulted in advanced cell function, and memory restoration in animal models have also benefited a few patients (Ramakrishna et al. 2011).
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.
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.
Efficient simulations of stretch growth axon based on improved HH model
Published in Neurological Research, 2023
Xiao Li, Xianxin Dong, Xikai Tu, Hailong Huang
Neuronal cell is composed of three components: a cell body, an axon, and a dendrite. These components are responsible for receiving, integrating, and delivering information. In general, neurons receive and integrate information from other neurons via their dendrites and cell bodies, and then transfer it to other neurons via their axons. Nerve fibers have great excitability and conductivity, and their primary role is to transmit information between neurons. When a sufficient stimulus excites a nerve fiber, it immediately generates a propagable action potential. Chemical synapses allow action potentials to be passed from one neuron to the next by transporting neurotransmitters through synaptic vesicles. The action potential-induced shift in membrane potential causes the calcium channel on the synaptic terminal membrane to open, allowing a substantial number of calcium ions to flow into the membrane, resulting in an abrupt increase in calcium ions in the synaptic membrane. When synaptic vesicles detect an increase in the number of calcium ions in the surrounding environment, they fuse with the presynaptic membrane and spit neurotransmitters into the synaptic gap. After binding to a protein receptor on the postsynaptic membrane, the neurotransmitter causes excitement or inhibition.
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.