The Experts below are selected from a list of 539622 Experts worldwide ranked by ideXlab platform
Christian Luscher - One of the best experts on this subject based on the ideXlab platform.
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contrasting forms of cocaine evoked plasticity Control Components of relapse
Nature, 2014Co-Authors: Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin C Oconnor, Christian LuscherAbstract:Nucleus accumbens neurons serve to integrate information from cortical and limbic regions to direct behaviour. Addictive drugs are proposed to hijack this system, enabling drug-associated cues to trigger relapse to drug seeking. However, the connections affected and proof of causality remain to be established. Here we use a mouse model of delayed cue-associated cocaine seeking with ex vivo electrophysiology in optogenetically delineated circuits. We find that seeking correlates with rectifying AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor transmission and a reduced AMPA/NMDA (N-methyl-d-aspartate) ratio at medial prefrontal cortex (mPFC) to nucleus accumbens shell D1-receptor medium-sized spiny neurons (D1R-MSNs). In contrast, the AMPA/NMDA ratio increases at ventral hippocampus to D1R-MSNs. Optogenetic reversal of cocaine-evoked plasticity at both inputs abolishes seeking, whereas selective reversal at mPFC or ventral hippocampus synapses impairs response discrimination or reduces response vigour during seeking, respectively. Taken together, we describe how information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Our approach holds promise for identifying synaptic causalities in other behavioural disorders. Information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Addictive drugs are thought to hijack the neural circuits in integrative brain centres, such as the nucleus accumbens, that send signals to various brain regions to Control behavioural responses. Drug-associated cues can become powerful triggers of drug-seeking behaviour because of such manipulations, increasing the chance of relapse after the cessation of drug-taking. Here Christian Luscher and colleagues identify cocaine-evoked alterations to specific neural pathways in projections from the prefrontal cortex or ventral hippocampus that interact with separate dopaminergic populations in the nucleus accumbens of mice. Manipulation of drug-induced plasticity within both these pathways abolishes drug-seeking behaviour, whereas disrupting plasticity in just one pathway impairs drug-response discrimination or the vigour of cue responses. These findings reveal the plasticity mechanisms underlying information integration at the nucleus accumbens and show how drugs like cocaine can alter this plasticity to permit relapse.
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contrasting forms of cocaine evoked plasticity Control Components of relapse
Nature, 2014Co-Authors: Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin C Oconnor, Christian LuscherAbstract:Information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse.
Emmanuel Valjent - One of the best experts on this subject based on the ideXlab platform.
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contrasting forms of cocaine evoked plasticity Control Components of relapse
Nature, 2014Co-Authors: Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin C Oconnor, Christian LuscherAbstract:Nucleus accumbens neurons serve to integrate information from cortical and limbic regions to direct behaviour. Addictive drugs are proposed to hijack this system, enabling drug-associated cues to trigger relapse to drug seeking. However, the connections affected and proof of causality remain to be established. Here we use a mouse model of delayed cue-associated cocaine seeking with ex vivo electrophysiology in optogenetically delineated circuits. We find that seeking correlates with rectifying AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor transmission and a reduced AMPA/NMDA (N-methyl-d-aspartate) ratio at medial prefrontal cortex (mPFC) to nucleus accumbens shell D1-receptor medium-sized spiny neurons (D1R-MSNs). In contrast, the AMPA/NMDA ratio increases at ventral hippocampus to D1R-MSNs. Optogenetic reversal of cocaine-evoked plasticity at both inputs abolishes seeking, whereas selective reversal at mPFC or ventral hippocampus synapses impairs response discrimination or reduces response vigour during seeking, respectively. Taken together, we describe how information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Our approach holds promise for identifying synaptic causalities in other behavioural disorders. Information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Addictive drugs are thought to hijack the neural circuits in integrative brain centres, such as the nucleus accumbens, that send signals to various brain regions to Control behavioural responses. Drug-associated cues can become powerful triggers of drug-seeking behaviour because of such manipulations, increasing the chance of relapse after the cessation of drug-taking. Here Christian Luscher and colleagues identify cocaine-evoked alterations to specific neural pathways in projections from the prefrontal cortex or ventral hippocampus that interact with separate dopaminergic populations in the nucleus accumbens of mice. Manipulation of drug-induced plasticity within both these pathways abolishes drug-seeking behaviour, whereas disrupting plasticity in just one pathway impairs drug-response discrimination or the vigour of cue responses. These findings reveal the plasticity mechanisms underlying information integration at the nucleus accumbens and show how drugs like cocaine can alter this plasticity to permit relapse.
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contrasting forms of cocaine evoked plasticity Control Components of relapse
Nature, 2014Co-Authors: Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin C Oconnor, Christian LuscherAbstract:Information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse.
Julie Espallergues - One of the best experts on this subject based on the ideXlab platform.
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contrasting forms of cocaine evoked plasticity Control Components of relapse
Nature, 2014Co-Authors: Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin C Oconnor, Christian LuscherAbstract:Nucleus accumbens neurons serve to integrate information from cortical and limbic regions to direct behaviour. Addictive drugs are proposed to hijack this system, enabling drug-associated cues to trigger relapse to drug seeking. However, the connections affected and proof of causality remain to be established. Here we use a mouse model of delayed cue-associated cocaine seeking with ex vivo electrophysiology in optogenetically delineated circuits. We find that seeking correlates with rectifying AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor transmission and a reduced AMPA/NMDA (N-methyl-d-aspartate) ratio at medial prefrontal cortex (mPFC) to nucleus accumbens shell D1-receptor medium-sized spiny neurons (D1R-MSNs). In contrast, the AMPA/NMDA ratio increases at ventral hippocampus to D1R-MSNs. Optogenetic reversal of cocaine-evoked plasticity at both inputs abolishes seeking, whereas selective reversal at mPFC or ventral hippocampus synapses impairs response discrimination or reduces response vigour during seeking, respectively. Taken together, we describe how information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Our approach holds promise for identifying synaptic causalities in other behavioural disorders. Information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Addictive drugs are thought to hijack the neural circuits in integrative brain centres, such as the nucleus accumbens, that send signals to various brain regions to Control behavioural responses. Drug-associated cues can become powerful triggers of drug-seeking behaviour because of such manipulations, increasing the chance of relapse after the cessation of drug-taking. Here Christian Luscher and colleagues identify cocaine-evoked alterations to specific neural pathways in projections from the prefrontal cortex or ventral hippocampus that interact with separate dopaminergic populations in the nucleus accumbens of mice. Manipulation of drug-induced plasticity within both these pathways abolishes drug-seeking behaviour, whereas disrupting plasticity in just one pathway impairs drug-response discrimination or the vigour of cue responses. These findings reveal the plasticity mechanisms underlying information integration at the nucleus accumbens and show how drugs like cocaine can alter this plasticity to permit relapse.
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contrasting forms of cocaine evoked plasticity Control Components of relapse
Nature, 2014Co-Authors: Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin C Oconnor, Christian LuscherAbstract:Information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse.
Yuelin Zhang - One of the best experts on this subject based on the ideXlab platform.
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RESEARCH ARTICLE ER Quality Control Components UGGT and STT3a Are Required for Activation of Defense Responses in Bir1-1
2016Co-Authors: Qian Zhang, Tongjun Sun, Yuelin ZhangAbstract:The receptor-like kinase SUPPRESSOR OF BIR1, 1 (SOBIR1) functions as a critical regu-lator in plant immunity. It is required for activation of cell death and defense responses in Arabidopsis bak1-interacting receptor-like kinase 1,1 (bir1-1) mutant plants. Here we report that the ER quality Control component UDP-glucose:glycoprotein glucosyltransferase (UGGT) is required for the biogenesis of SOBIR1 and mutations in UGGT suppress the spontaneous cell death and constitutive defense responses in bir1-1. Loss of function of STT3a, which encodes a subunit of the oligosaccharyltransferase complex, also sup-presses the autoimmune phenotype in bir1-1. However, it has no effect on the accumulation of SOBIR1, suggesting that additional signaling Components other than SOBIR1 may be regulated by ER quality Control. Our study provides clear evidence that ER quality Control play critical roles in regulating defense activation in bir1-1
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ER quality Control Components UGGT and STT3a are required for activation of defense responses in bir1-1.
PloS one, 2015Co-Authors: Qian Zhang, Tongjun Sun, Yuelin ZhangAbstract:The receptor-like kinase SUPPRESSOR OF BIR1, 1 (SOBIR1) functions as a critical regulator in plant immunity. It is required for activation of cell death and defense responses in Arabidopsis bak1-interacting receptor-like kinase 1,1 (bir1-1) mutant plants. Here we report that the ER quality Control component UDP-glucose:glycoprotein glucosyltransferase (UGGT) is required for the biogenesis of SOBIR1 and mutations in UGGT suppress the spontaneous cell death and constitutive defense responses in bir1-1. Loss of function of STT3a, which encodes a subunit of the oligosaccharyltransferase complex, also suppresses the autoimmune phenotype in bir1-1. However, it has no effect on the accumulation of SOBIR1, suggesting that additional signaling Components other than SOBIR1 may be regulated by ER quality Control. Our study provides clear evidence that ER quality Control play critical roles in regulating defense activation in bir1-1.
Vincent Pascoli - One of the best experts on this subject based on the ideXlab platform.
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contrasting forms of cocaine evoked plasticity Control Components of relapse
Nature, 2014Co-Authors: Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin C Oconnor, Christian LuscherAbstract:Nucleus accumbens neurons serve to integrate information from cortical and limbic regions to direct behaviour. Addictive drugs are proposed to hijack this system, enabling drug-associated cues to trigger relapse to drug seeking. However, the connections affected and proof of causality remain to be established. Here we use a mouse model of delayed cue-associated cocaine seeking with ex vivo electrophysiology in optogenetically delineated circuits. We find that seeking correlates with rectifying AMPA (α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) receptor transmission and a reduced AMPA/NMDA (N-methyl-d-aspartate) ratio at medial prefrontal cortex (mPFC) to nucleus accumbens shell D1-receptor medium-sized spiny neurons (D1R-MSNs). In contrast, the AMPA/NMDA ratio increases at ventral hippocampus to D1R-MSNs. Optogenetic reversal of cocaine-evoked plasticity at both inputs abolishes seeking, whereas selective reversal at mPFC or ventral hippocampus synapses impairs response discrimination or reduces response vigour during seeking, respectively. Taken together, we describe how information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Our approach holds promise for identifying synaptic causalities in other behavioural disorders. Information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse. Addictive drugs are thought to hijack the neural circuits in integrative brain centres, such as the nucleus accumbens, that send signals to various brain regions to Control behavioural responses. Drug-associated cues can become powerful triggers of drug-seeking behaviour because of such manipulations, increasing the chance of relapse after the cessation of drug-taking. Here Christian Luscher and colleagues identify cocaine-evoked alterations to specific neural pathways in projections from the prefrontal cortex or ventral hippocampus that interact with separate dopaminergic populations in the nucleus accumbens of mice. Manipulation of drug-induced plasticity within both these pathways abolishes drug-seeking behaviour, whereas disrupting plasticity in just one pathway impairs drug-response discrimination or the vigour of cue responses. These findings reveal the plasticity mechanisms underlying information integration at the nucleus accumbens and show how drugs like cocaine can alter this plasticity to permit relapse.
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contrasting forms of cocaine evoked plasticity Control Components of relapse
Nature, 2014Co-Authors: Vincent Pascoli, Jean Terrier, Julie Espallergues, Emmanuel Valjent, Eoin C Oconnor, Christian LuscherAbstract:Information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse.