Drug abuse, brain calcification and glutamate-induced neurodegeneration

Positive and negative reinforcing systems are part of the mechanism of drug dependence. Drugs with abuse potential may change the manner of response to negative emotional stimuli, activate positive emotional reactions and possess primary reinforcing properties. Catecholaminergic and peptidergic proc...

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Autores: Rodríguez Allué, Manuel José, Pugliese, Marco, Mahy Gehenne, Josette Nicole
Tipo de recurso: artículo
Estado:Versión aceptada para publicación
Fecha de publicación:2009
País:España
Institución:Universidad de Barcelona
Repositorio:Dipòsit Digital de la UB
OAI Identifier:oai:diposit.ub.edu:2445/34290
Acceso en línea:https://hdl.handle.net/2445/34290
Access Level:acceso abierto
Palabra clave:Àcid glutàmic
Aminoàcids
Malalties neurodegeneratives
Drogues
Glutamic acid
Amino acids
Neurodegenerative Diseases
Drugs of abuse
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spelling Drug abuse, brain calcification and glutamate-induced neurodegenerationRodríguez Allué, Manuel JoséPugliese, MarcoMahy Gehenne, Josette NicoleÀcid glutàmicAminoàcidsMalalties neurodegenerativesDroguesGlutamic acidAmino acidsNeurodegenerative DiseasesDrugs of abusePositive and negative reinforcing systems are part of the mechanism of drug dependence. Drugs with abuse potential may change the manner of response to negative emotional stimuli, activate positive emotional reactions and possess primary reinforcing properties. Catecholaminergic and peptidergic processes are of importance in these mechanisms. Current research needs to understand the types of adaptations that underlie the particularly long-lived aspects of addiction. Presently, glutamate is candidate to play a role in the enduring effects of drugs of abuse. For example, it participates in the chronic pathological changes of corticostriatal terminals produced by methamphetamine. At the synaptic level, a link between over-activation of glutamate receptors, [C(a2+)](i) increase and neuronal damage has been clearly established leading to neurodegeneration. Thus, neurodegeneration can start after an acute over-stimulation whose immediate effects depend on a diversity of calcium-activated mechanisms. If sufficient, the initial insult results in calcification and activation of a chronic on-going process with a progressive loss of neurons. At present, long-term effects of drug dependence underlie an excitotoxicity process linked to a polysynaptic pathway that dynamically regulates synaptic glutamate. Retaliatory mechanisms include energy capability of the neurons, inhibitory systems and cytoplasmic calcium precipitation as part of the neuron-glia interactions. This paper presents an integrated view of these molecular and cellular mechanisms to help understand their relationship and interdependence in a chronic pathological process that suggest new targets for therapeutic intervention.Bentham Science Publishers2009info:eu-repo/semantics/articleinfo:eu-repo/semantics/acceptedVersionapplication/pdfhttps://hdl.handle.net/2445/34290Articles publicats en revistes (Ciències Fisiològiques)reponame:Dipòsit Digital de la UBinstname:Universidad de BarcelonaInglésVersió postprint del document publicat a: http://dx.doi.org/10.2174/1874473711205040004Current Drug Abuse Reviews, 2009, vol. 2, num. 1, p. 99-112http://dx.doi.org/10.2174/1874473711205040004(c) Bentham Science Publishers, 2009info:eu-repo/semantics/openAccessoai:diposit.ub.edu:2445/342902026-05-27T06:46:51Z
dc.title.none.fl_str_mv Drug abuse, brain calcification and glutamate-induced neurodegeneration
title Drug abuse, brain calcification and glutamate-induced neurodegeneration
spellingShingle Drug abuse, brain calcification and glutamate-induced neurodegeneration
Rodríguez Allué, Manuel José
Àcid glutàmic
Aminoàcids
Malalties neurodegeneratives
Drogues
Glutamic acid
Amino acids
Neurodegenerative Diseases
Drugs of abuse
title_short Drug abuse, brain calcification and glutamate-induced neurodegeneration
title_full Drug abuse, brain calcification and glutamate-induced neurodegeneration
title_fullStr Drug abuse, brain calcification and glutamate-induced neurodegeneration
title_full_unstemmed Drug abuse, brain calcification and glutamate-induced neurodegeneration
title_sort Drug abuse, brain calcification and glutamate-induced neurodegeneration
dc.creator.none.fl_str_mv Rodríguez Allué, Manuel José
Pugliese, Marco
Mahy Gehenne, Josette Nicole
author Rodríguez Allué, Manuel José
author_facet Rodríguez Allué, Manuel José
Pugliese, Marco
Mahy Gehenne, Josette Nicole
author_role author
author2 Pugliese, Marco
Mahy Gehenne, Josette Nicole
author2_role author
author
dc.subject.none.fl_str_mv Àcid glutàmic
Aminoàcids
Malalties neurodegeneratives
Drogues
Glutamic acid
Amino acids
Neurodegenerative Diseases
Drugs of abuse
topic Àcid glutàmic
Aminoàcids
Malalties neurodegeneratives
Drogues
Glutamic acid
Amino acids
Neurodegenerative Diseases
Drugs of abuse
description Positive and negative reinforcing systems are part of the mechanism of drug dependence. Drugs with abuse potential may change the manner of response to negative emotional stimuli, activate positive emotional reactions and possess primary reinforcing properties. Catecholaminergic and peptidergic processes are of importance in these mechanisms. Current research needs to understand the types of adaptations that underlie the particularly long-lived aspects of addiction. Presently, glutamate is candidate to play a role in the enduring effects of drugs of abuse. For example, it participates in the chronic pathological changes of corticostriatal terminals produced by methamphetamine. At the synaptic level, a link between over-activation of glutamate receptors, [C(a2+)](i) increase and neuronal damage has been clearly established leading to neurodegeneration. Thus, neurodegeneration can start after an acute over-stimulation whose immediate effects depend on a diversity of calcium-activated mechanisms. If sufficient, the initial insult results in calcification and activation of a chronic on-going process with a progressive loss of neurons. At present, long-term effects of drug dependence underlie an excitotoxicity process linked to a polysynaptic pathway that dynamically regulates synaptic glutamate. Retaliatory mechanisms include energy capability of the neurons, inhibitory systems and cytoplasmic calcium precipitation as part of the neuron-glia interactions. This paper presents an integrated view of these molecular and cellular mechanisms to help understand their relationship and interdependence in a chronic pathological process that suggest new targets for therapeutic intervention.
publishDate 2009
dc.date.none.fl_str_mv 2009
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/acceptedVersion
format article
status_str acceptedVersion
dc.identifier.none.fl_str_mv https://hdl.handle.net/2445/34290
url https://hdl.handle.net/2445/34290
dc.language.none.fl_str_mv Inglés
language_invalid_str_mv Inglés
dc.relation.none.fl_str_mv Versió postprint del document publicat a: http://dx.doi.org/10.2174/1874473711205040004
Current Drug Abuse Reviews, 2009, vol. 2, num. 1, p. 99-112
http://dx.doi.org/10.2174/1874473711205040004
dc.rights.none.fl_str_mv (c) Bentham Science Publishers, 2009
info:eu-repo/semantics/openAccess
rights_invalid_str_mv (c) Bentham Science Publishers, 2009
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Bentham Science Publishers
publisher.none.fl_str_mv Bentham Science Publishers
dc.source.none.fl_str_mv Articles publicats en revistes (Ciències Fisiològiques)
reponame:Dipòsit Digital de la UB
instname:Universidad de Barcelona
instname_str Universidad de Barcelona
reponame_str Dipòsit Digital de la UB
collection Dipòsit Digital de la UB
repository.name.fl_str_mv
repository.mail.fl_str_mv
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score 15,300724

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