Synaptic Pathophysiology and Treatment of Lambert-Eaton Myasthenic Syndrome.
Identifieur interne : 000160 ( PubMed/Corpus ); précédent : 000159; suivant : 000161Synaptic Pathophysiology and Treatment of Lambert-Eaton Myasthenic Syndrome.
Auteurs : Tyler B. Tarr ; Peter Wipf ; Stephen D. MerineySource :
- Molecular neurobiology [ 1559-1182 ] ; 2015.
English descriptors
- KwdEn :
- Animals, Humans, Lambert-Eaton Myasthenic Syndrome (drug therapy), Lambert-Eaton Myasthenic Syndrome (physiopathology), Lambert-Eaton Myasthenic Syndrome (therapy), Neuromuscular Junction (drug effects), Neuromuscular Junction (physiopathology), Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Synapses (drug effects), Synapses (pathology).
- MESH :
- chemical , pharmacology : Neuroprotective Agents.
- drug effects : Neuromuscular Junction, Synapses.
- drug therapy : Lambert-Eaton Myasthenic Syndrome.
- pathology : Synapses.
- physiopathology : Lambert-Eaton Myasthenic Syndrome, Neuromuscular Junction.
- chemical , therapeutic use : Neuroprotective Agents.
- therapy : Lambert-Eaton Myasthenic Syndrome.
- Animals, Humans.
Abstract
Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease that disrupts the normally reliable neurotransmission at the neuromuscular junction (NMJ). This disruption is thought to result from an autoantibody-mediated removal of a subset of the P/Q-type Ca(2+) channels involved with neurotransmitter release. With less neurotransmitter release at the NMJ, LEMS patients experience debilitating muscle weakness. The underlying cause of LEMS in slightly more than half of all patients is small cell lung cancer, and cancer therapy is the priority for these patients. In the remaining cases, the cause of LEMS is unknown, and these patients often rely on symptomatic treatment options, as there is no cure. However, current symptomatic treatment options, such as 3,4-diaminopyridine (3,4-DAP), can have significant dose-limiting side effects; thus, additional treatment approaches would benefit LEMS patients. Recent studies introduced a novel Ca(2+) channel agonist (GV-58) as a potential therapeutic alternative for LEMS. Additionally, this work has shown that GV-58 and 3,4-DAP interact in a supra-additive manner to completely restore the magnitude of neurotransmitter release at the NMJs of a LEMS mouse model. In this review, we discuss synaptic mechanisms for reliability at the NMJ and how these mechanisms are disrupted in LEMS. We then discuss the current treatment options for LEMS patients, while also considering recent work demonstrating the therapeutic potential of GV-58 alone and in combination with 3,4-DAP.
DOI: 10.1007/s12035-014-8887-2
PubMed: 25195700
Links to Exploration step
pubmed:25195700Le document en format XML
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Meriney</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2015">2015</date><idno type="RBID">pubmed:25195700</idno><idno type="pmid">25195700</idno><idno type="doi">10.1007/s12035-014-8887-2</idno><idno type="wicri:Area/PubMed/Corpus">000160</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000160</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Synaptic Pathophysiology and Treatment of Lambert-Eaton Myasthenic Syndrome.</title><author><name sortKey="Tarr, Tyler B" sort="Tarr, Tyler B" uniqKey="Tarr T" first="Tyler B" last="Tarr">Tyler B. Tarr</name><affiliation><nlm:affiliation>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, 15260, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Wipf, Peter" sort="Wipf, Peter" uniqKey="Wipf P" first="Peter" last="Wipf">Peter Wipf</name></author><author><name sortKey="Meriney, Stephen D" sort="Meriney, Stephen D" uniqKey="Meriney S" first="Stephen D" last="Meriney">Stephen D. Meriney</name></author></analytic><series><title level="j">Molecular neurobiology</title><idno type="eISSN">1559-1182</idno><imprint><date when="2015" type="published">2015</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Humans</term><term>Lambert-Eaton Myasthenic Syndrome (drug therapy)</term><term>Lambert-Eaton Myasthenic Syndrome (physiopathology)</term><term>Lambert-Eaton Myasthenic Syndrome (therapy)</term><term>Neuromuscular Junction (drug effects)</term><term>Neuromuscular Junction (physiopathology)</term><term>Neuroprotective Agents (pharmacology)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Synapses (drug effects)</term><term>Synapses (pathology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Neuromuscular Junction</term><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lambert-Eaton Myasthenic Syndrome</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Synapses</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lambert-Eaton Myasthenic Syndrome</term><term>Neuromuscular Junction</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Lambert-Eaton Myasthenic Syndrome</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease that disrupts the normally reliable neurotransmission at the neuromuscular junction (NMJ). This disruption is thought to result from an autoantibody-mediated removal of a subset of the P/Q-type Ca(2+) channels involved with neurotransmitter release. With less neurotransmitter release at the NMJ, LEMS patients experience debilitating muscle weakness. The underlying cause of LEMS in slightly more than half of all patients is small cell lung cancer, and cancer therapy is the priority for these patients. In the remaining cases, the cause of LEMS is unknown, and these patients often rely on symptomatic treatment options, as there is no cure. However, current symptomatic treatment options, such as 3,4-diaminopyridine (3,4-DAP), can have significant dose-limiting side effects; thus, additional treatment approaches would benefit LEMS patients. Recent studies introduced a novel Ca(2+) channel agonist (GV-58) as a potential therapeutic alternative for LEMS. Additionally, this work has shown that GV-58 and 3,4-DAP interact in a supra-additive manner to completely restore the magnitude of neurotransmitter release at the NMJs of a LEMS mouse model. In this review, we discuss synaptic mechanisms for reliability at the NMJ and how these mechanisms are disrupted in LEMS. We then discuss the current treatment options for LEMS patients, while also considering recent work demonstrating the therapeutic potential of GV-58 alone and in combination with 3,4-DAP.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25195700</PMID><DateCreated><Year>2015</Year><Month>07</Month><Day>22</Day></DateCreated><DateCompleted><Year>2016</Year><Month>05</Month><Day>17</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1559-1182</ISSN><JournalIssue CitedMedium="Internet"><Volume>52</Volume><Issue>1</Issue><PubDate><Year>2015</Year><Month>Aug</Month></PubDate></JournalIssue><Title>Molecular neurobiology</Title><ISOAbbreviation>Mol. Neurobiol.</ISOAbbreviation></Journal><ArticleTitle>Synaptic Pathophysiology and Treatment of Lambert-Eaton Myasthenic Syndrome.</ArticleTitle><Pagination><MedlinePgn>456-63</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s12035-014-8887-2</ELocationID><Abstract><AbstractText>Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disease that disrupts the normally reliable neurotransmission at the neuromuscular junction (NMJ). This disruption is thought to result from an autoantibody-mediated removal of a subset of the P/Q-type Ca(2+) channels involved with neurotransmitter release. With less neurotransmitter release at the NMJ, LEMS patients experience debilitating muscle weakness. The underlying cause of LEMS in slightly more than half of all patients is small cell lung cancer, and cancer therapy is the priority for these patients. In the remaining cases, the cause of LEMS is unknown, and these patients often rely on symptomatic treatment options, as there is no cure. However, current symptomatic treatment options, such as 3,4-diaminopyridine (3,4-DAP), can have significant dose-limiting side effects; thus, additional treatment approaches would benefit LEMS patients. Recent studies introduced a novel Ca(2+) channel agonist (GV-58) as a potential therapeutic alternative for LEMS. Additionally, this work has shown that GV-58 and 3,4-DAP interact in a supra-additive manner to completely restore the magnitude of neurotransmitter release at the NMJs of a LEMS mouse model. In this review, we discuss synaptic mechanisms for reliability at the NMJ and how these mechanisms are disrupted in LEMS. We then discuss the current treatment options for LEMS patients, while also considering recent work demonstrating the therapeutic potential of GV-58 alone and in combination with 3,4-DAP.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tarr</LastName><ForeName>Tyler B</ForeName><Initials>TB</Initials><AffiliationInfo><Affiliation>Department of Neuroscience, Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA, 15260, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Wipf</LastName><ForeName>Peter</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Meriney</LastName><ForeName>Stephen D</ForeName><Initials>SD</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P50 GM067082</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>GM067082</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH 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