Prefrontal synaptic markers of cocaine addiction-like behavior in rats.
Identifieur interne : 001564 ( Main/Corpus ); précédent : 001563; suivant : 001565Prefrontal synaptic markers of cocaine addiction-like behavior in rats.
Auteurs : F. Kasanetz ; M. Lafourcade ; V. Deroche-Gamonet ; J-M Revest ; N. Berson ; E. Balado ; J-F Fiancette ; P. Renault ; P-V Piazza ; O J ManzoniSource :
- Molecular psychiatry [ 1476-5578 ] ; 2013.
English descriptors
- KwdEn :
- Amino Acids (pharmacology), Analysis of Variance (MeSH), Animals (MeSH), Biophysics (MeSH), Bridged Bicyclo Compounds, Heterocyclic (pharmacology), Cocaine (administration & dosage), Cocaine (adverse effects), Conditioning, Operant (drug effects), Disease Models, Animal (MeSH), Dopamine Uptake Inhibitors (administration & dosage), Dopamine Uptake Inhibitors (adverse effects), Electric Stimulation (MeSH), Excitatory Amino Acid Agonists (pharmacology), Excitatory Postsynaptic Potentials (drug effects), In Vitro Techniques (MeSH), Long-Term Synaptic Depression (drug effects), Male (MeSH), Patch-Clamp Techniques (MeSH), Prefrontal Cortex (metabolism), Prefrontal Cortex (pathology), Psychiatric Status Rating Scales (MeSH), Rats (MeSH), Rats, Sprague-Dawley (MeSH), Receptors, AMPA (metabolism), Receptors, N-Methyl-D-Aspartate (metabolism), Self Administration (MeSH), Substance-Related Disorders (metabolism), Substance-Related Disorders (pathology), Substance-Related Disorders (psychology), Synapses (drug effects), Synapses (metabolism).
- MESH :
- chemical , administration & dosage : Cocaine, Dopamine Uptake Inhibitors.
- chemical , adverse effects : Cocaine, Dopamine Uptake Inhibitors.
- chemical , metabolism : Receptors, AMPA, Receptors, N-Methyl-D-Aspartate.
- chemical , pharmacology : Amino Acids, Bridged Bicyclo Compounds, Heterocyclic, Excitatory Amino Acid Agonists.
- drug effects : Conditioning, Operant, Excitatory Postsynaptic Potentials, Long-Term Synaptic Depression, Synapses.
- metabolism : Prefrontal Cortex, Substance-Related Disorders, Synapses.
- pathology : Prefrontal Cortex, Substance-Related Disorders.
- psychology : Substance-Related Disorders.
- Analysis of Variance, Animals, Biophysics, Disease Models, Animal, Electric Stimulation, In Vitro Techniques, Male, Patch-Clamp Techniques, Psychiatric Status Rating Scales, Rats, Rats, Sprague-Dawley, Self Administration.
Abstract
Defining the drug-induced neuroadaptations specifically associated with the behavioral manifestation of addiction is a daunting task. To address this issue, we used a behavioral model that differentiates rats controlling their drug use (Non-Addict-like) from rats undergoing transition to addiction (Addict-like). Dysfunctions in prefrontal cortex (PFC) synaptic circuits are thought to be responsible for the loss of control over drug taking that characterizes addicted individuals. Here, we studied the synaptic alterations in prelimbic PFC (pPFC) circuits associated with transition to addiction. We discovered that some of the changes induced by cocaine self-administration (SA), such as the impairment of the endocannabinoid-mediated long-term synaptic depression (eCB-LTD) was similarly abolished in Non-Addict- and Addict-like rats and thus unrelated to transition to addiction. In contrast, metabotropic glutamate receptor 2/3-mediated LTD (mGluR2/3-LTD) was specifically suppressed in Addict-like rats, which also show a concomitant postsynaptic plasticity expressed as a change in the relative contribution of AMPAR and NMDAR to basal glutamate-mediated synaptic transmission. Addiction-associated synaptic alterations in the pPFC were not fully developed at early stages of cocaine SA, when addiction-like behaviors are still absent, suggesting that pathological behaviors appear once the pPFC is compromised. These data identify specific synaptic impairments in the pPFC associated with addiction and support the idea that alterations of synaptic plasticity are core markers of drug dependence.
DOI: 10.1038/mp.2012.59
PubMed: 22584869
Links to Exploration step
pubmed:22584869Le document en format XML
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<front><div type="abstract" xml:lang="en">Defining the drug-induced neuroadaptations specifically associated with the behavioral manifestation of addiction is a daunting task. To address this issue, we used a behavioral model that differentiates rats controlling their drug use (Non-Addict-like) from rats undergoing transition to addiction (Addict-like). Dysfunctions in prefrontal cortex (PFC) synaptic circuits are thought to be responsible for the loss of control over drug taking that characterizes addicted individuals. Here, we studied the synaptic alterations in prelimbic PFC (pPFC) circuits associated with transition to addiction. We discovered that some of the changes induced by cocaine self-administration (SA), such as the impairment of the endocannabinoid-mediated long-term synaptic depression (eCB-LTD) was similarly abolished in Non-Addict- and Addict-like rats and thus unrelated to transition to addiction. In contrast, metabotropic glutamate receptor 2/3-mediated LTD (mGluR2/3-LTD) was specifically suppressed in Addict-like rats, which also show a concomitant postsynaptic plasticity expressed as a change in the relative contribution of AMPAR and NMDAR to basal glutamate-mediated synaptic transmission. Addiction-associated synaptic alterations in the pPFC were not fully developed at early stages of cocaine SA, when addiction-like behaviors are still absent, suggesting that pathological behaviors appear once the pPFC is compromised. These data identify specific synaptic impairments in the pPFC associated with addiction and support the idea that alterations of synaptic plasticity are core markers of drug dependence.</div>
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<Abstract><AbstractText>Defining the drug-induced neuroadaptations specifically associated with the behavioral manifestation of addiction is a daunting task. To address this issue, we used a behavioral model that differentiates rats controlling their drug use (Non-Addict-like) from rats undergoing transition to addiction (Addict-like). Dysfunctions in prefrontal cortex (PFC) synaptic circuits are thought to be responsible for the loss of control over drug taking that characterizes addicted individuals. Here, we studied the synaptic alterations in prelimbic PFC (pPFC) circuits associated with transition to addiction. We discovered that some of the changes induced by cocaine self-administration (SA), such as the impairment of the endocannabinoid-mediated long-term synaptic depression (eCB-LTD) was similarly abolished in Non-Addict- and Addict-like rats and thus unrelated to transition to addiction. In contrast, metabotropic glutamate receptor 2/3-mediated LTD (mGluR2/3-LTD) was specifically suppressed in Addict-like rats, which also show a concomitant postsynaptic plasticity expressed as a change in the relative contribution of AMPAR and NMDAR to basal glutamate-mediated synaptic transmission. Addiction-associated synaptic alterations in the pPFC were not fully developed at early stages of cocaine SA, when addiction-like behaviors are still absent, suggesting that pathological behaviors appear once the pPFC is compromised. These data identify specific synaptic impairments in the pPFC associated with addiction and support the idea that alterations of synaptic plasticity are core markers of drug dependence.</AbstractText>
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