Role of the ERK/MSK1 signalling pathway in chromatin remodelling and brain responses to drugs of abuse DOI Open Access
Karen Brami‐Cherrier, Emmanuel Roze, Jean‐Antoine Girault

et al.

Journal of Neurochemistry, Journal Year: 2009, Volume and Issue: 108(6), P. 1323 - 1335

Published: Jan. 12, 2009

Abstract Drugs of abuse induce neuroadaptations through regulation gene expression. Although much attention has focused on transcription factor activities, new concepts have recently emerged the role chromatin remodelling as a prerequisite for expression in neurons. Thus, to occur, must be decondensed, dynamic process that depends post‐translational modifications histones. We review here these with particular emphasis histone H3 phosphorylation at promoter specific genes, including c‐ fos and jun . trace signalling pathways involved provide evidence mitogen stress‐activated protein kinase‐1 (MSK1) downstream from MAPK/extracellular‐signal regulated kinase (ERK) cascade. In response cocaine, MSK1 controls an early phase striatal action may potentiated by concomitant inhibition phosphatase 1 nuclear translocation dopamine‐ cAMP‐regulated phosphoprotein Mr = 32 000. is critically transcription, cocaine‐induced locomotor sensitization. ERK plays dual drug addiction direct activation factors remodelling.

Language: Английский

REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade DOI
Thomas Tzschentke

Addiction Biology, Journal Year: 2007, Volume and Issue: 12(3-4), P. 227 - 462

Published: July 30, 2007

ABSTRACT Conditioned place preference (CPP) continues to be one of the most popular models study motivational effects drugs and non‐drug treatments in experimental animals. This is obvious from a steady year‐to‐year increase number publications reporting use this model. Since compilation preceding review 1998, more than 1000 new studies using conditioning have been published, aim present provide an overview these recent publications. There are trends developments that literature last decade. First, as knockout transgenic animals become available, increasingly used assess or rewards genetically modified Second, there still small but growing on aspects pain, field pre‐clinical research has so far received little attention, because lack appropriate animal models. Third, widely tolerance sensitization rewarding induced by pre‐treatment regimens. Fourth, extinction/reinstatement procedures becoming popular. interesting approach thought model certain relapse addictive behavior previously almost exclusively studied drug self‐administration paradigms. It now also established provides additional technically easy important phenomenon. The enormous covered prevented in‐depth discussion many methodological, pharmacological neurobiological aspects; large extent, presentation data had limited short condensed summary relevant findings.

Language: Английский

Citations

1295

Molecular mechanisms of memory reconsolidation DOI
Natalie C. Tronson, Jane R. Taylor

Nature reviews. Neuroscience, Journal Year: 2007, Volume and Issue: 8(4), P. 262 - 275

Published: March 7, 2007

Language: Английский

Citations

769

Opposing Patterns of Signaling Activation in Dopamine D1and D2Receptor-Expressing Striatal Neurons in Response to Cocaine and Haloperidol DOI Creative Commons
Jesus Bertran‐Gonzalez, Clémentine Bosch‐Bouju, Matthieu Maroteaux

et al.

Journal of Neuroscience, Journal Year: 2008, Volume and Issue: 28(22), P. 5671 - 5685

Published: May 28, 2008

Psychostimulants and other drugs of abuse activate extracellular signal-regulated kinase (ERK) in the striatum, through combined stimulation dopamine D 1 receptors (D1Rs) glutamate NMDA receptors. Antipsychotic similar signaling proteins striatum by blocking 2 (D2Rs). However, neurons which these pathways are activated psychotropic not precisely identified. We used transgenic mice, enhanced green fluorescent protein (EGFP) expression was driven D1R promoter ( drd1a -EGFP) or D2R drd2 -EGFP). confirmed -EGFP striatonigral striatopallidal neurons. Drd2 also expressed cholinergic interneurons, whereas no either detected GABAergic interneurons. Acute cocaine treatment increased phosphorylation ERK its direct indirect nuclear targets, mitogen- stress-activated kinase-1 (MSK1) histone H3, exclusively D1R-expressing output dorsal nucleus accumbens. Cocaine-induced c-Fos Zif268 predominated but observed D2R-expressing One week after repeated administration, cocaine-induced responses were decreased, with exception striatum. The remained confined to In contrast, acute haloperidol injection ERK, MSK1, H3 only induced c-fos zif268 predominantly Our results demonstrate that specifically two completely segregated populations striatal neurons, providing evidence for selective mechanisms exert their long-term effects.

Language: Английский

Citations

586

Neuroplasticity in the mesolimbic dopamine system and cocaine addiction DOI
Mark J. Thomas, Peter W. Kalivas, Yavin Shaham

et al.

British Journal of Pharmacology, Journal Year: 2008, Volume and Issue: 154(2), P. 327 - 342

Published: March 17, 2008

The main characteristics of cocaine addiction are compulsive drug use despite adverse consequences and high rates relapse during periods abstinence. A current popular hypothesis is that due to drug-induced neuroadaptations in reward-related learning memory processes, which cause hypersensitivity cocaine-associated cues, impulsive decision making abnormal habit-like learned behaviours insensitive consequences. Here, we review results from studies on the effect exposure selected signalling cascades, growth factors physiological processes previously implicated neuroplasticity underlying normal memory. These include extracellular signal-regulated kinase (ERK) pathway, brain-derived neurotrophic factor (BDNF), glutamate transmission, synaptic plasticity (primarily form long-term potentiation depression, LTP LTD). We also discuss degree these cocaine-induced changes mesolimbic dopamine system mediate psychomotor sensitization cocaine-seeking behaviours, as assessed animal models addiction. Finally, speculate how may interact initiate sustain seeking.

Language: Английский

Citations

508

ERK2: a logical AND gate critical for drug-induced plasticity? DOI
Jean‐Antoine Girault, Emmanuel Valjent, Jocelyne Caboche

et al.

Current Opinion in Pharmacology, Journal Year: 2006, Volume and Issue: 7(1), P. 77 - 85

Published: Nov. 8, 2006

Language: Английский

Citations

339

Consolidation and Reconsolidation: Two Lives of Memories? DOI Creative Commons
Sam McKenzie, Howard Eichenbaum

Neuron, Journal Year: 2011, Volume and Issue: 71(2), P. 224 - 233

Published: July 1, 2011

Language: Английский

Citations

326

Neural and psychological mechanisms underlying compulsive drug seeking habits and drug memories – indications for novel treatments of addiction DOI Creative Commons
Barry J. Everitt

European Journal of Neuroscience, Journal Year: 2014, Volume and Issue: 40(1), P. 2163 - 2182

Published: June 17, 2014

Abstract This review discusses the evidence for hypothesis that development of drug addiction can be understood in terms interactions between Pavlovian and instrumental learning memory mechanisms brain underlie seeking taking drugs. It is argued these behaviours initially are goal‐directed, but increasingly become elicited as stimulus–response habits by drug‐associated conditioned stimuli established conditioning. further compulsive use emerges result a loss prefrontal cortical inhibitory control over habits. Data reviewed indicate transitions from to abuse depend upon shifts ventral dorsal striatal behaviour, mediated part serial connectivity striatum midbrain dopamine systems. Only some individuals lose their use, importance behavioural impulsivity vulnerability trait predicting stimulant animals humans, together with consideration an emerging neuroendophenotype discussed. Finally, potential developing treatments considered light neuropsychological advances reviewed, including possibility targeting reconsolidation extinction reduce influences on means promoting abstinence preventing relapse.

Language: Английский

Citations

294

The Role of Reconsolidation and the Dynamic Process of Long-Term Memory Formation and Storage DOI Creative Commons
Cristina M. Alberini

Frontiers in Behavioral Neuroscience, Journal Year: 2011, Volume and Issue: 5

Published: Jan. 1, 2011

It is becoming increasingly clear that the processes of memory formation and storage are exquisitely dynamic. Elucidating nature temporal evolution biological changes accompany encoding, storage, retrieval key to understand formation. For explicit or medial lobe-dependent memories form after a discrete event stored for long time, physical underlying encoding processing information (memory trace engram) remain in fragile state some time. However, over new becomes resistant disruption until it consolidated. Retrieval reactivation an apparently consolidated can render labile again, reconsolidation process occurs mediate its restabilization. Reconsolidation also evolves with age memory: Young sensitive post-reactivation disruption, but older more resistant. Why does become again if retrieved reactivated? Here I suggest main function contribute lingering consolidation strengthening. discuss literature results regarding influence passage time on memory. These points have important implications use therapeutic settings.

Language: Английский

Citations

267

The persistence of maladaptive memory: Addiction, drug memories and anti-relapse treatments DOI
Amy Milton, Barry J. Everitt

Neuroscience & Biobehavioral Reviews, Journal Year: 2012, Volume and Issue: 36(4), P. 1119 - 1139

Published: Jan. 29, 2012

Language: Английский

Citations

256

The roles of protein kinases in learning and memory DOI Open Access
Karl-Peter Giese, Keiko Mizuno

Learning & Memory, Journal Year: 2013, Volume and Issue: 20(10), P. 540 - 552

Published: Sept. 16, 2013

In the adult mammalian brain, more than 250 protein kinases are expressed, but only a few of these currently known to enable learning and memory. Based on this information it appears that memory-related either impact synaptic transmission by altering ion channel properties or density, regulate gene expression synthesis causing structural changes at existing synapses as well synaptogenesis. Here, we review roles in short-term memory formation, consolidation, storage, retrieval, reconsolidation, extinction. Specifically, discuss calcium/calmodulin-dependent kinase II (CaMKII), calcium/calmodulin cascade, extracellular signal regulated 1 2 (ERK1/2), cAMP-dependent A (PKA), cGMP-dependent G (PKG), phosphatidylinositol 3-kinase (PI3K) pathway, M ζ (PKMζ). Although important for processes, much remains be learned how they act. Therefore, will identify characterize critical phosphorylation substrates so sophisticated understanding processes achieved. This also allow systematic analysis dysfunctional activity mental disorders.

Language: Английский

Citations

230