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The patient with acute neurological problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Most synapses are chemical; neurotransmitters are used to bridge the gap between the terminal bouton and the post-synaptic structure (see Figure 9.6). Neurotransmitters released from the presynaptic terminal diffuse across the synaptic cleft and bind to the post-synaptic terminal, where they inhibit or excite the post-synaptic structure. Inhibition blocks the post-synaptic structure, and excitation stimulates the post-synaptic structure.
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.
Radiation Damage of the Nervous System
Published in Kedar N. Prasad, Handbook of RADIOBIOLOGY, 2020
The neuron is subdivided according to anatomical and functional criteria. The perikaryon includes and surrounds the nucleus, and contains most of the cytoplasmic organelles. The dendrites and axons arise from the perikaryon. At its end, the axon splits into branches, each forming a presynaptic terminal. The various parts of a neuron show differential radiation response.
Neurological manifestations of SARS-CoV-2 infections: towards quantum dots based management approaches
Published in Journal of Drug Targeting, 2023
Faezeh Almasi, Fatemeh Mohammadipanah
Based on retrograde transportation theory, the released virus from presynaptic terminal enters the postsynaptic neurons via receptor mediated endocytosis and some facilitator proteins like kinesin and dynein. One of the probable retrograde pathways of SARS-CoV-2 entry to CNS is the olfactory pathway. Results suggest that SARS-CoV-2 like other human COVs prefers the intranasal invasion via the olfactory route [86]. Recently, Sungnak et al. demonstrated the gene expression patterns of ACE2 and TMPRSS2 as the main entry factors of SARS-CoV-2 which are at the highest level in the examined nasal epithelial cells [87]. The olfactory pathway has been well established for neurotropic respiratory viruses, mainly CoVs, but further and precise investigation for neuroinvasion of SARS-CoV-2 is demanded.
Abnormal larval neuromuscular junction morphology and physiology in Drosophila prickle isoform mutants with known axonal transport defects and adult seizure behavior
Published in Journal of Neurogenetics, 2022
Atsushi Ueda, Tristan C. D. G. O’Harrow, Xiaomin Xing, Salleh Ehaideb, J. Robert Manak, Chun-Fang Wu
To enable analysis of presynaptic terminal excitability, we also performed electrotonic stimulation on the NMJ (Ganetzky & Wu, 1982, 1983; Wu et al., 1978). Briefly, tetrodotoxin (TTX, 3 µM) was applied to block Na+ channels. To achieve direct electrotonic stimulation of the terminal, a longer duration (2-ms) stimulus was applied near the hemisegment entry point by drawing in the segmental nerve to the suction pipette, so as to effectively control different levels of depolarization with passive electrotonic spreading to the terminal. In this manner, synaptic terminal CaV channels were directly triggered by local depolarization, independent from invasion of axonal Na+ action potentials (Wu et al., 1978). For the generation of plateau EJPs, multiple K+ channel types in presynaptic terminals, including Shaker (Kv1; Jan, Jan, & Dennis, 1977), Shab (Kv2; Ueda & Wu, 2006) and eag ( Kv10; Ganetzky & Wu, 1982, 1983) were blocked by application of 4-aminopyridine (4-AP) and tetraethylammonium (TEA) to allow the development of full-blown regenerative Ca2+-action potentials that sustain prolonged transmitter release (Lee, Ueda, & Wu, 2014; Ueda & Wu, 2009).
In vitro models of neuromuscular junctions and their potential for novel drug discovery and development
Published in Expert Opinion on Drug Discovery, 2020
Olaia F Vila, Yihuai Qu, Gordana Vunjak-Novakovic
The neuromuscular junction (NMJ) is the chemical synapse between a motoneuron and a skeletal muscle fiber that enables muscle contraction and allows for voluntary motor movement. NMJ formation is controlled by interactions between motoneurons, skeletal muscle fibers, and glial cells [1]. In vertebrates, the presynaptic motor nerve terminal dictates the synthesis, storage, and release of the neurotransmitter acetylcholine (ACh) and agrin [2]. When an action potential reaches the presynaptic terminal and activates voltage-gated calcium channels, calcium enters the neuron and triggers the diffusion of ACh across the synaptic cleft to the acetylcholine receptors (AChRs) on the postsynaptic muscle membrane. Activation of these receptors leads to opening of cation channels in the muscle membrane, producing its depolarization. Meanwhile, acetylcholinesterases located within the synaptic cleft degrade the acetylcholine, allowing the NMJ to return to its resting state.