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Relevant bibliographies by topics / Acetylcholine; Transmission; Lambert-Eaton

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Academic literature on the topic 'Acetylcholine; Transmission; Lambert-Eaton'

Author: Grafiati

Published: 4 June 2021

Last updated: 15 February 2022

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Journal articles on the topic "Acetylcholine; Transmission; Lambert-Eaton"

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Giannoccaro, Maria Pia, Patrizia Avoni, and Rocco Liguori. "Presynaptic Paraneoplastic Disorders of the Neuromuscular Junction: An Update." Brain Sciences 11, no. 8 (2021): 1035. http://dx.doi.org/10.3390/brainsci11081035.

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The neuromuscular junction (NMJ) is the target of a variety of immune-mediated disorders, usually classified as presynaptic and postsynaptic, according to the site of the antigenic target and consequently of the neuromuscular transmission alteration. Although less common than the classical autoimmune postsynaptic myasthenia gravis, presynaptic disorders are important to recognize due to the frequent association with cancer. Lambert Eaton myasthenic syndrome is due to a presynaptic failure to release acetylcholine, caused by antibodies to the presynaptic voltage-gated calcium channels. Acquired

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Rodríguez Cruz, Pedro M., Judith Cossins, David Beeson, and Angela Vincent. "The Neuromuscular Junction in Health and Disease: Molecular Mechanisms Governing Synaptic Formation and Homeostasis." Frontiers in Molecular Neuroscience 13 (December 3, 2020). http://dx.doi.org/10.3389/fnmol.2020.610964.

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The neuromuscular junction (NMJ) is a highly specialized synapse between a motor neuron nerve terminal and its muscle fiber that are responsible for converting electrical impulses generated by the motor neuron into electrical activity in the muscle fibers. On arrival of the motor nerve action potential, calcium enters the presynaptic terminal, which leads to the release of the neurotransmitter acetylcholine (ACh). ACh crosses the synaptic gap and binds to ACh receptors (AChRs) tightly clustered on the surface of the muscle fiber; this leads to the endplate potential which initiates the muscle

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3

Totzeck, Andreas, Petra Mummel, Oliver Kastrup, and Tim Hagenacker. "Clinical features of neuromuscular disorders in patients with N-type voltage-gated calcium channel antibodies." European Journal of Translational Myology 26, no. 4 (2016). http://dx.doi.org/10.4081/ejtm.2016.5962.

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Neuromuscular junction disorders affect the pre- or postsynaptic nerve to muscle transmission due to autoimmune antibodies. Members of the group like myasthenia gravis and Lambert-Eaton syndrome have pathophysiologically distinct characteristics. However, in practice, distinction may be difficult. We present a series of three patients with a myasthenic syndrome, dropped-head syndrome, bulbar and respiratory muscle weakness and positive testing for anti-N-type voltage-gated calcium channel antibodies. In two cases anti-acetylcholin receptor antibodies were elevated, anti-P/Q-type voltage-gated

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Dissertations / Theses on the topic "Acetylcholine; Transmission; Lambert-Eaton"

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Giovannini, Federica. "Voltage-dependent calcium channel subtypes at the mouse neuromuscular junction : evidence for the role of a resistant component." Thesis, University of Oxford, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365445.

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Dulin, Renaud. "La 4-aminopyridine et la 3,4-diaminopyridine : propriétés pharmacologiques, statut, utilisations thérapeutiques." Bordeaux 2, 1999. http://www.theses.fr/1999BOR2P063.

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Books on the topic "Acetylcholine; Transmission; Lambert-Eaton"

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Reddy, Ugan, and Nicholas Hirsch. Diagnosis, assessment, and management of myasthenia gravis and paramyasthenic syndromes. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0244.

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Diseases that affect the neuromuscular junction (NMJ) interfere with normal nerve transmission and cause weakness of voluntary muscles. The two most commonly encountered are acquired myasthenia gravis (MG) and the Lambert–Eaton myasthenic syndrome (LEMS). Acquired MG is an autoimmune disease in which antibodies are directed towards receptors at the NMJ. In 85% of patients, IgG antibodies against the postsynaptic acetylcholine receptor (AChR) are found (seropositive MG). The thymus gland appears to be involved in the production of these which cause an increase rate of degradation of AChR result

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