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Mechanisms of locomotor sensitization to drugs of abuse in a two-injection protocol.

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TLDR
TIPS in mouse is a context-dependent response, which involves an increase in extracellular dopamine, stimulation of D1 and NMDA receptors, regulation of the cAMP-dependent and ERK pathways, inhibition of PP1, and protein synthesis.
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This article is published in Neuropsychopharmacology.The article was published on 2010-01-01 and is currently open access. It has received 194 citations till now. The article focuses on the topics: Sensitization & Anisomycin.

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The Nucleus Accumbens: Mechanisms of Addiction across Drug Classes Reflect the Importance of Glutamate Homeostasis.

TL;DR: A review of the literature describing how synaptic plasticity in the accumbens is altered after exposure to drugs of abuse and withdrawal and also how pharmacological manipulation of glutamate systems in the Accumbens can inhibit drug seeking in the laboratory setting is provided.
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Reversal of cocaine-evoked synaptic potentiation resets drug-induced adaptive behaviour

TL;DR: These findings establish synaptic potentiation selectively in D1R-MSNs as a mechanism underlying a core component of addiction, probably by creating an imbalance between distinct populations of MSNs in the nucleus accumbens, and provide proof of principle that reversal of cocaine-evoked synaptic plasticity can treat behavioural alterations caused by addictive drugs.
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Refining deep brain stimulation to emulate optogenetic treatment of synaptic pathology

TL;DR: It is discovered that acute low-frequency DBS, refined by selective blockade of dopamine D1 receptors, mimics optogenetic mGluR-dependent normalization of synaptic transmission, and there was a long-lasting abolishment of behavioral sensitization.
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What is the Degree of Segregation between Striatonigral and Striatopallidal Projections

TL;DR: In this paper, the authors review classical and recent studies supporting the segregation of striatonigral and striatopallidal neurons and discuss the anatomical and functional evidence challenging some aspects of this segregation and outline questions that are still to be addressed.
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Cyclic Adenosine Monophosphate–Independent Tyrosine Phosphorylation of NR2B Mediates Cocaine-Induced Extracellular Signal-Regulated Kinase Activation

TL;DR: A new cyclic adenosine monophosphate-independent pathway responsible for the integration of dopamine and glutamate signals by the ERK cascade in the striatum and for long-term behavioral alterations induced by cocaine is highlighted.
References
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The neural basis of drug craving: An incentive-sensitization theory of addiction

TL;DR: S sensitization of incentive salience can produce addictive behavior even if the expectation of drug pleasure or the aversive properties of withdrawal are diminished and even in the face of strong disincentives, including the loss of reputation, job, home and family.
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Dopamine transmission in the initiation and expression of drug- and stress-induced sensitization of motor activity

TL;DR: It is found that the dopamine neurons of sensitized animals have become increasingly sensitive to excitatory pharmacological and environmental stimuli or desensitized to inhibitory regulation, and changes in cellular activity or protein synthesis may result in a change in the presynaptic regulation of axon terminal dopamine release.
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Alterations in dopaminergic and glutamatergic transmission in the induction and expression of behavioral sensitization: a critical review of preclinical studies.

TL;DR: The distinctions between drugs in the induction and expression of sensitization indicate that behavioral sensitization can arise from multiple neuroadaptations in multiple brain nuclei, not only the result of distinct molecular targets for the drugs, but may also include a differential involvement of learned associations.
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Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons

TL;DR: It is shown that a prominent form of synaptic plasticity can be elicited by a single in vivo exposure to cocaine and therefore may be involved in the early stages of the development of drug addiction.
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Neuroadaptation. Incubation of cocaine craving after withdrawal.

TL;DR: Behavioural evidence is provided from laboratory animals suggesting that the onset of craving is delayed and that craving does not decay, but rather increases progressively, over a two-month withdrawal period.
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