Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment

The glutamate system is involved in many aspects of neuronal synaptic strength and function during development and throughout life. Synapse formation in early brain development, synapse maintenance, and synaptic plasticity are all influenced by the glutamate system. The number of neurons and the num...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Pharmacology & therapeutics (Oxford) 2003-02, Vol.97 (2), p.153-179
Hauptverfasser: Konradi, Christine, Heckers, Stephan
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 179
container_issue 2
container_start_page 153
container_title Pharmacology & therapeutics (Oxford)
container_volume 97
creator Konradi, Christine
Heckers, Stephan
description The glutamate system is involved in many aspects of neuronal synaptic strength and function during development and throughout life. Synapse formation in early brain development, synapse maintenance, and synaptic plasticity are all influenced by the glutamate system. The number of neurons and the number of their connections are determined by the activity of the glutamate system and its receptors. Malfunctions of the glutamate system affect neuroplasticity and can cause neuronal toxicity. In schizophrenia, many glutamate-regulated processes seem to be perturbed. Abnormal neuronal development, abnormal synaptic plasticity, and neurodegeneration have been proposed to be causal or contributing factors in schizophrenia. Interestingly, it seems that the glutamate system is dysregulated and that N-methyl- d-aspartate receptors operate at reduced activity. Here we discuss how the molecular aspects of glutamate malfunction can explain some of the neuropathology observed in schizophrenia, and how the available treatment intervenes through the glutamate system.
doi_str_mv 10.1016/S0163-7258(02)00328-5
format Article
fullrecord <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4203361</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0163725802003285</els_id><sourcerecordid>12559388</sourcerecordid><originalsourceid>FETCH-LOGICAL-c515t-60245ae36749ba2efbcae80efb3a622ef88c123602d4a1130e4c268353cbebc43</originalsourceid><addsrcrecordid>eNqFUEtLAzEQDqJorf4EJUc9rOax2aYeFCm-QPGggidDNjvbRnY3S7It1F9v-qDqycsMw_diPoSOKDmjhGbnL3HwZMCEPCHslBDOZCK2UI_KwTCJ2Ps26m0oe2g_hE9CSJoStov2KBNiyKXsoY8nV4GZVtpjHVowXcCuxONq2ulad4CLefAwjnhnXXOBbd1W1iyPgEvncTAT--XaiYfGaqybAtto0XnQXQ1Nd4B2Sl0FOFzvPnq7vXkd3SePz3cPo-vHxAgquiQjLBUaeDZIh7lmUOZGgyRxc52xeEtpKOORVqSaUk4gNSyTXHCTQ25S3keXK992mtdQmBjtdaVab2vt58ppq_4ijZ2osZuplBHOMxoNxMrAeBfiy-VGS4laFK6WhatFm4owtSxciag7_h38o1o3HAlXKwLE92cWvArGQmOgsD7WrQpn_4n4BqEslBc</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment</title><source>MEDLINE</source><source>Access via ScienceDirect (Elsevier)</source><creator>Konradi, Christine ; Heckers, Stephan</creator><creatorcontrib>Konradi, Christine ; Heckers, Stephan</creatorcontrib><description>The glutamate system is involved in many aspects of neuronal synaptic strength and function during development and throughout life. Synapse formation in early brain development, synapse maintenance, and synaptic plasticity are all influenced by the glutamate system. The number of neurons and the number of their connections are determined by the activity of the glutamate system and its receptors. Malfunctions of the glutamate system affect neuroplasticity and can cause neuronal toxicity. In schizophrenia, many glutamate-regulated processes seem to be perturbed. Abnormal neuronal development, abnormal synaptic plasticity, and neurodegeneration have been proposed to be causal or contributing factors in schizophrenia. Interestingly, it seems that the glutamate system is dysregulated and that N-methyl- d-aspartate receptors operate at reduced activity. Here we discuss how the molecular aspects of glutamate malfunction can explain some of the neuropathology observed in schizophrenia, and how the available treatment intervenes through the glutamate system.</description><identifier>ISSN: 0163-7258</identifier><identifier>EISSN: 1879-016X</identifier><identifier>DOI: 10.1016/S0163-7258(02)00328-5</identifier><identifier>PMID: 12559388</identifier><language>eng</language><publisher>England: Elsevier Inc</publisher><subject>Antipsychotic Agents - pharmacology ; Antipsychotic Agents - therapeutic use ; Antipsychotic drugs ; Glutamate ; Glutamates - metabolism ; Glutamates - physiology ; Glutamates - therapeutic use ; Humans ; Neuropathology ; Neuroplasticity ; Neurotoxicity ; Neurotransmitter Agents - physiology ; Receptors, Glutamate - classification ; Receptors, Glutamate - physiology ; Receptors, Glutamate - therapeutic use ; Receptors, N-Methyl-D-Aspartate - drug effects ; Receptors, N-Methyl-D-Aspartate - physiology ; Schizophrenia ; Schizophrenia - drug therapy ; Schizophrenia - etiology ; Schizophrenia - pathology ; Signal Transduction - drug effects</subject><ispartof>Pharmacology &amp; therapeutics (Oxford), 2003-02, Vol.97 (2), p.153-179</ispartof><rights>2002 Elsevier Science Inc.</rights><rights>Copyright 2002 Elsevier Science Inc.</rights><rights>2002 Elsevier Science Inc. All rights reserved. 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c515t-60245ae36749ba2efbcae80efb3a622ef88c123602d4a1130e4c268353cbebc43</citedby><cites>FETCH-LOGICAL-c515t-60245ae36749ba2efbcae80efb3a622ef88c123602d4a1130e4c268353cbebc43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/S0163-7258(02)00328-5$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,780,784,885,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12559388$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Konradi, Christine</creatorcontrib><creatorcontrib>Heckers, Stephan</creatorcontrib><title>Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment</title><title>Pharmacology &amp; therapeutics (Oxford)</title><addtitle>Pharmacol Ther</addtitle><description>The glutamate system is involved in many aspects of neuronal synaptic strength and function during development and throughout life. Synapse formation in early brain development, synapse maintenance, and synaptic plasticity are all influenced by the glutamate system. The number of neurons and the number of their connections are determined by the activity of the glutamate system and its receptors. Malfunctions of the glutamate system affect neuroplasticity and can cause neuronal toxicity. In schizophrenia, many glutamate-regulated processes seem to be perturbed. Abnormal neuronal development, abnormal synaptic plasticity, and neurodegeneration have been proposed to be causal or contributing factors in schizophrenia. Interestingly, it seems that the glutamate system is dysregulated and that N-methyl- d-aspartate receptors operate at reduced activity. Here we discuss how the molecular aspects of glutamate malfunction can explain some of the neuropathology observed in schizophrenia, and how the available treatment intervenes through the glutamate system.</description><subject>Antipsychotic Agents - pharmacology</subject><subject>Antipsychotic Agents - therapeutic use</subject><subject>Antipsychotic drugs</subject><subject>Glutamate</subject><subject>Glutamates - metabolism</subject><subject>Glutamates - physiology</subject><subject>Glutamates - therapeutic use</subject><subject>Humans</subject><subject>Neuropathology</subject><subject>Neuroplasticity</subject><subject>Neurotoxicity</subject><subject>Neurotransmitter Agents - physiology</subject><subject>Receptors, Glutamate - classification</subject><subject>Receptors, Glutamate - physiology</subject><subject>Receptors, Glutamate - therapeutic use</subject><subject>Receptors, N-Methyl-D-Aspartate - drug effects</subject><subject>Receptors, N-Methyl-D-Aspartate - physiology</subject><subject>Schizophrenia</subject><subject>Schizophrenia - drug therapy</subject><subject>Schizophrenia - etiology</subject><subject>Schizophrenia - pathology</subject><subject>Signal Transduction - drug effects</subject><issn>0163-7258</issn><issn>1879-016X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFUEtLAzEQDqJorf4EJUc9rOax2aYeFCm-QPGggidDNjvbRnY3S7It1F9v-qDqycsMw_diPoSOKDmjhGbnL3HwZMCEPCHslBDOZCK2UI_KwTCJ2Ps26m0oe2g_hE9CSJoStov2KBNiyKXsoY8nV4GZVtpjHVowXcCuxONq2ulad4CLefAwjnhnXXOBbd1W1iyPgEvncTAT--XaiYfGaqybAtto0XnQXQ1Nd4B2Sl0FOFzvPnq7vXkd3SePz3cPo-vHxAgquiQjLBUaeDZIh7lmUOZGgyRxc52xeEtpKOORVqSaUk4gNSyTXHCTQ25S3keXK992mtdQmBjtdaVab2vt58ppq_4ijZ2osZuplBHOMxoNxMrAeBfiy-VGS4laFK6WhatFm4owtSxciag7_h38o1o3HAlXKwLE92cWvArGQmOgsD7WrQpn_4n4BqEslBc</recordid><startdate>20030201</startdate><enddate>20030201</enddate><creator>Konradi, Christine</creator><creator>Heckers, Stephan</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20030201</creationdate><title>Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment</title><author>Konradi, Christine ; Heckers, Stephan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c515t-60245ae36749ba2efbcae80efb3a622ef88c123602d4a1130e4c268353cbebc43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Antipsychotic Agents - pharmacology</topic><topic>Antipsychotic Agents - therapeutic use</topic><topic>Antipsychotic drugs</topic><topic>Glutamate</topic><topic>Glutamates - metabolism</topic><topic>Glutamates - physiology</topic><topic>Glutamates - therapeutic use</topic><topic>Humans</topic><topic>Neuropathology</topic><topic>Neuroplasticity</topic><topic>Neurotoxicity</topic><topic>Neurotransmitter Agents - physiology</topic><topic>Receptors, Glutamate - classification</topic><topic>Receptors, Glutamate - physiology</topic><topic>Receptors, Glutamate - therapeutic use</topic><topic>Receptors, N-Methyl-D-Aspartate - drug effects</topic><topic>Receptors, N-Methyl-D-Aspartate - physiology</topic><topic>Schizophrenia</topic><topic>Schizophrenia - drug therapy</topic><topic>Schizophrenia - etiology</topic><topic>Schizophrenia - pathology</topic><topic>Signal Transduction - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Konradi, Christine</creatorcontrib><creatorcontrib>Heckers, Stephan</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Pharmacology &amp; therapeutics (Oxford)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Konradi, Christine</au><au>Heckers, Stephan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment</atitle><jtitle>Pharmacology &amp; therapeutics (Oxford)</jtitle><addtitle>Pharmacol Ther</addtitle><date>2003-02-01</date><risdate>2003</risdate><volume>97</volume><issue>2</issue><spage>153</spage><epage>179</epage><pages>153-179</pages><issn>0163-7258</issn><eissn>1879-016X</eissn><abstract>The glutamate system is involved in many aspects of neuronal synaptic strength and function during development and throughout life. Synapse formation in early brain development, synapse maintenance, and synaptic plasticity are all influenced by the glutamate system. The number of neurons and the number of their connections are determined by the activity of the glutamate system and its receptors. Malfunctions of the glutamate system affect neuroplasticity and can cause neuronal toxicity. In schizophrenia, many glutamate-regulated processes seem to be perturbed. Abnormal neuronal development, abnormal synaptic plasticity, and neurodegeneration have been proposed to be causal or contributing factors in schizophrenia. Interestingly, it seems that the glutamate system is dysregulated and that N-methyl- d-aspartate receptors operate at reduced activity. Here we discuss how the molecular aspects of glutamate malfunction can explain some of the neuropathology observed in schizophrenia, and how the available treatment intervenes through the glutamate system.</abstract><cop>England</cop><pub>Elsevier Inc</pub><pmid>12559388</pmid><doi>10.1016/S0163-7258(02)00328-5</doi><tpages>27</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0163-7258
ispartof Pharmacology & therapeutics (Oxford), 2003-02, Vol.97 (2), p.153-179
issn 0163-7258
1879-016X
language eng
recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4203361
source MEDLINE; Access via ScienceDirect (Elsevier)
subjects Antipsychotic Agents - pharmacology
Antipsychotic Agents - therapeutic use
Antipsychotic drugs
Glutamate
Glutamates - metabolism
Glutamates - physiology
Glutamates - therapeutic use
Humans
Neuropathology
Neuroplasticity
Neurotoxicity
Neurotransmitter Agents - physiology
Receptors, Glutamate - classification
Receptors, Glutamate - physiology
Receptors, Glutamate - therapeutic use
Receptors, N-Methyl-D-Aspartate - drug effects
Receptors, N-Methyl-D-Aspartate - physiology
Schizophrenia
Schizophrenia - drug therapy
Schizophrenia - etiology
Schizophrenia - pathology
Signal Transduction - drug effects
title Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-22T04%3A53%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmed_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Molecular%20aspects%20of%20glutamate%20dysregulation:%20implications%20for%20schizophrenia%20and%20its%20treatment&rft.jtitle=Pharmacology%20&%20therapeutics%20(Oxford)&rft.au=Konradi,%20Christine&rft.date=2003-02-01&rft.volume=97&rft.issue=2&rft.spage=153&rft.epage=179&rft.pages=153-179&rft.issn=0163-7258&rft.eissn=1879-016X&rft_id=info:doi/10.1016/S0163-7258(02)00328-5&rft_dat=%3Cpubmed_cross%3E12559388%3C/pubmed_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/12559388&rft_els_id=S0163725802003285&rfr_iscdi=true