Cocaine-induced adaptations in D1 and D2 accumbens projection neurons (a dichotomy not necessarily synonymous with direct and indirect pathways).
TLDR
Cocaine exposure causes enduring neuroadaptations in ventral striatum, or nucleus accumbens (NAc), an area critically involved in reward learning and relapse of drug seeking, including changes to synaptic plasticity, glutamatergic signaling, and spine morphology.About:
This article is published in Current Opinion in Neurobiology.The article was published on 2013-08-01 and is currently open access. It has received 240 citations till now. The article focuses on the topics: Nucleus accumbens & Medium spiny neuron.read more
Citations
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Journal ArticleDOI
The Brain on Drugs: From Reward to Addiction.
Nora D. Volkow,Marisela Morales +1 more
TL;DR: The circuit- and cell-level mechanisms of addiction are discussed and interventions designed to mitigate or even reverse them would be beneficial for the treatment of addiction.
Journal ArticleDOI
The Nucleus Accumbens: Mechanisms of Addiction across Drug Classes Reflect the Importance of Glutamate Homeostasis.
Michael D. Scofield,Jasper A. Heinsbroek,Cassandra D. Gipson,Yonatan M. Kupchik,Sade Spencer,Alexander C.W. Smith,Douglas Roberts-Wolfe,P. W. Kalivas +7 more
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.
Journal ArticleDOI
Coding the direct/indirect pathways by D1 and D2 receptors is not valid for accumbens projections
Yonatan M. Kupchik,Yonatan M. Kupchik,Robyn M Brown,Robyn M Brown,Jasper A. Heinsbroek,Mary Kay Lobo,Danielle J. Schwartz,Peter W. Kalivas +7 more
TL;DR: It is found that current thinking attributing D1 and D2 selectivity to accumbens projections akin to dorsal striatal pathways needs to be reconsidered.
Journal ArticleDOI
Contrasting forms of cocaine-evoked plasticity control components of relapse
Vincent Pascoli,Jean Terrier,Julie Espallergues,Emmanuel Valjent,Eoin C. O'Connor,Christian Lüscher +5 more
TL;DR: How information integration in the nucleus accumbens is commandeered by cocaine at discrete synapses to allow relapse is described and holds promise for identifying synaptic causalities in other behavioural disorders.
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Synaptic mechanisms underlying persistent cocaine craving
TL;DR: Rodent studies of cue-induced cocaine craving during abstinence are discussed, with a focus on neuronal plasticity in the reward circuitry that maintains high levels of craving.
References
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Neurocircuitry of Addiction
George F. Koob,Nora D. Volkow +1 more
TL;DR: The delineation of the neurocircuitry of the evolving stages of the addiction syndrome forms a heuristic basis for the search for the molecular, genetic, and neuropharmacological neuroadaptations that are key to vulnerability for developing and maintaining addiction.
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Modulation of Striatal Projection Systems by Dopamine
TL;DR: The contrast provided by these studies has provided new insights into how the striatum responds to fluctuations in DA signaling and how diseases that alter this signaling change striatal function.
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Specificity in the projection patterns of accumbal core and shell in the rat.
TL;DR: The efferent projections of the core and shell areas of the nucleus accumbens were studied with a combination of anterograde and retrograde tract-tracing methods, including Phaseolus vulgaris-leucoagglutinin, horseradish peroxidase and fluorescent tracers.
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The glutamate homeostasis hypothesis of addiction
TL;DR: The hierarchy of corticostriatal information processing that normally permits the prefrontal cortex to regulate reinforcement-seeking behaviours is impaired by chronic drug use and some of these pathological changes are amenable to new glutamate- and neuroplasticity-based pharmacotherapies for treating addiction.
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Dichotomous Dopaminergic Control of Striatal Synaptic Plasticity
TL;DR: DA plays complementary roles in these two types of MSN to ensure that synaptic plasticity is bidirectional and Hebbian, leading to unidirectional changes in plasticity that could underlie network pathology and symptoms in Parkinson's disease.