Recent insights into the mode of action of memantine and ketamine.
Identifieur interne : 000714 ( PubMed/Curation ); précédent : 000713; suivant : 000715Recent insights into the mode of action of memantine and ketamine.
Auteurs : Jon W. Johnson [États-Unis] ; Nathan G. Glasgow [États-Unis] ; Nadezhda V. Povysheva [États-Unis]Source :
- Current opinion in pharmacology [ 1471-4973 ] ; 2015.
Descripteurs français
- KwdFr :
- MESH :
- antagonistes et inhibiteurs : Récepteurs du N-méthyl-D-aspartate.
- pharmacologie : Antagonistes des acides aminés excitateurs, Kétamine, Mémantine.
- Animaux, Conception de médicament, Humains, Thérapie moléculaire ciblée.
English descriptors
- KwdEn :
- MESH :
- chemical , antagonists & inhibitors : Receptors, N-Methyl-D-Aspartate.
- chemical , pharmacology : Excitatory Amino Acid Antagonists, Ketamine, Memantine.
- Animals, Drug Design, Humans, Molecular Targeted Therapy.
Abstract
The clinical benefits of the glutamate receptor antagonists memantine and ketamine have helped sustain optimism that glutamate receptors represent viable targets for development of therapeutic drugs. Both memantine and ketamine antagonize N-methyl-D-aspartate receptors (NMDARs), a glutamate receptor subfamily, by blocking the receptor-associated ion channel. Although many of the basic characteristics of NMDAR inhibition by memantine and ketamine appear similar, their effects on humans and to a lesser extent on rodents are strongly divergent. Some recent research suggests that preferential inhibition by memantine and ketamine of distinct NMDAR subpopulations may contribute to the drugs' differential clinical effects. Here we review studies that shed light on possible explanations for differences between the effects of memantine and ketamine.
DOI: 10.1016/j.coph.2014.11.006
PubMed: 25462293
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Glasgow</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neuroscience and Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience and Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260</wicri:regionArea></affiliation></author><author><name sortKey="Povysheva, Nadezhda V" sort="Povysheva, Nadezhda V" uniqKey="Povysheva N" first="Nadezhda V" last="Povysheva">Nadezhda V. Povysheva</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neuroscience and Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience and Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260</wicri:regionArea></affiliation></author></analytic><series><title level="j">Current opinion in pharmacology</title><idno type="eISSN">1471-4973</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>Drug Design</term><term>Excitatory Amino Acid Antagonists (pharmacology)</term><term>Humans</term><term>Ketamine (pharmacology)</term><term>Memantine (pharmacology)</term><term>Molecular Targeted Therapy</term><term>Receptors, N-Methyl-D-Aspartate (antagonists & inhibitors)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Antagonistes des acides aminés excitateurs (pharmacologie)</term><term>Conception de médicament</term><term>Humains</term><term>Kétamine (pharmacologie)</term><term>Mémantine (pharmacologie)</term><term>Récepteurs du N-méthyl-D-aspartate (antagonistes et inhibiteurs)</term><term>Thérapie moléculaire ciblée</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, N-Methyl-D-Aspartate</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Excitatory Amino Acid Antagonists</term><term>Ketamine</term><term>Memantine</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteurs du N-méthyl-D-aspartate</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antagonistes des acides aminés excitateurs</term><term>Kétamine</term><term>Mémantine</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Drug Design</term><term>Humans</term><term>Molecular Targeted Therapy</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Conception de médicament</term><term>Humains</term><term>Thérapie moléculaire ciblée</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The clinical benefits of the glutamate receptor antagonists memantine and ketamine have helped sustain optimism that glutamate receptors represent viable targets for development of therapeutic drugs. Both memantine and ketamine antagonize N-methyl-D-aspartate receptors (NMDARs), a glutamate receptor subfamily, by blocking the receptor-associated ion channel. Although many of the basic characteristics of NMDAR inhibition by memantine and ketamine appear similar, their effects on humans and to a lesser extent on rodents are strongly divergent. Some recent research suggests that preferential inhibition by memantine and ketamine of distinct NMDAR subpopulations may contribute to the drugs' differential clinical effects. Here we review studies that shed light on possible explanations for differences between the effects of memantine and ketamine.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25462293</PMID><DateCreated><Year>2015</Year><Month>02</Month><Day>04</Day></DateCreated><DateCompleted><Year>2015</Year><Month>09</Month><Day>28</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1471-4973</ISSN><JournalIssue CitedMedium="Internet"><Volume>20</Volume><PubDate><Year>2015</Year><Month>Feb</Month></PubDate></JournalIssue><Title>Current opinion in pharmacology</Title><ISOAbbreviation>Curr Opin Pharmacol</ISOAbbreviation></Journal><ArticleTitle>Recent insights into the mode of action of memantine and ketamine.</ArticleTitle><Pagination><MedlinePgn>54-63</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.coph.2014.11.006</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S1471-4892(14)00160-X</ELocationID><Abstract><AbstractText>The clinical benefits of the glutamate receptor antagonists memantine and ketamine have helped sustain optimism that glutamate receptors represent viable targets for development of therapeutic drugs. Both memantine and ketamine antagonize N-methyl-D-aspartate receptors (NMDARs), a glutamate receptor subfamily, by blocking the receptor-associated ion channel. Although many of the basic characteristics of NMDAR inhibition by memantine and ketamine appear similar, their effects on humans and to a lesser extent on rodents are strongly divergent. Some recent research suggests that preferential inhibition by memantine and ketamine of distinct NMDAR subpopulations may contribute to the drugs' differential clinical effects. Here we review studies that shed light on possible explanations for differences between the effects of memantine and ketamine.</AbstractText><CopyrightInformation>Copyright © 2014 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Johnson</LastName><ForeName>Jon W</ForeName><Initials>JW</Initials><AffiliationInfo><Affiliation>Department of Neuroscience and Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA. Electronic address: jjohnson@pitt.edu.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Glasgow</LastName><ForeName>Nathan G</ForeName><Initials>NG</Initials><AffiliationInfo><Affiliation>Department of Neuroscience and Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Povysheva</LastName><ForeName>Nadezhda V</ForeName><Initials>NV</Initials><AffiliationInfo><Affiliation>Department of Neuroscience and Center for Neuroscience, University of Pittsburgh, Pittsburgh, PA 15260, USA.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>T32 NS073548</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 MH045817</GrantID><Acronym>MH</Acronym><Agency>NIMH NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R41 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