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Open AccessJournal ArticleDOI

Distinct role of nucleus accumbens D2-MSN projections to ventral pallidum in different phases of motivated behavior

TLDR
In this paper , optogenetic modulation of D2-MSN to ventral pallidum (VP) projections during different stages of motivated behavior has contrasting effects in motivation; activation at reward delivery decreases motivation; optical inhibition triggers the opposite behavioral effect.
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This article is published in Cell Reports.The article was published on 2022-02-01 and is currently open access. It has received 15 citations till now. The article focuses on the topics: Optogenetics & Nucleus accumbens.

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Layer-specific pain relief pathways originating from primary motor cortex

TL;DR: Gan et al. as discussed by the authors found a connection from the M1 to the nucleus accumbens reward circuitry through a M1 layer 6-mediodorsal thalamus pathway, which specifically suppresses negative emotional valence and associated coping behaviors in neuropathic pain.
Journal ArticleDOI

Nucleus Accumbens Core Dopamine D2 Receptor-Expressing Neurons Control Reversal Learning but Not Set-Shifting in Behavioral Flexibility in Male Mice

TL;DR: It is suggested that NAc D2-MSNs play a critical role in suppressing responding toward specific learned cues that are now associated with unfavorable outcomes, but not in the suppression of more general learned strategies (i.e., in set-shifting).
Posted ContentDOI

Involvement of nucleus accumbens D2-MSN projections to the ventral pallidum in anxious-like behavior

TL;DR: The results suggest that D2-MSN-VP projections contribute for the development of anxious-like behavior, through modulation of GABAergic activity in the VP.
Journal ArticleDOI

Ventral pallidal regulation of motivated behaviors and reinforcement

TL;DR: The ventral pallidum (VP) is a central node of the ventral basal ganglia, and recent studies have revealed complex VP cellular heterogeneity and cell- and circuit-specific regulation of reward, aversion, motivation, and drug-seeking behaviors as mentioned in this paper .
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Ventral Subiculum Inputs to Nucleus Accumbens Medial Shell Preferentially Innervate D2R Medium Spiny Neurons and Contain Calcium Permeable AMPARs

TL;DR: This work systematically characterized the vSUB-NAcMS circuit with cell-type and synapse specific resolution in male and female mice and found that vSub output to dopamine receptor type-1 (D1R) and type-2 (D2R) expressing medium spiny neurons (MSNs) displays a functional connectivity bias for D2R MSNs.
References
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Journal ArticleDOI

A Neural Substrate of Prediction and Reward

TL;DR: Findings in this work indicate that dopaminergic neurons in the primate whose fluctuating output apparently signals changes or errors in the predictions of future salient and rewarding events can be understood through quantitative theories of adaptive optimizing control.
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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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Progressive ratio schedules in drug self-administration studies in rats: a method to evaluate reinforcing efficacy

TL;DR: This review addresses the technical, statistical, and theoretical issues related to the use of the PR schedule in self-administration studies in rats to examine psychostimulant and opiate reinforcement.
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Distinct roles for direct and indirect pathway striatal neurons in reinforcement

TL;DR: This work bypassed dopamine signaling itself and tested how optogenetic activation of dopamine D1 or D2 receptor–expressing striatal projection neurons influenced reinforcement learning in mice, indicating that activation of these circuits is sufficient to modify the probability of performing future actions.
Journal ArticleDOI

Cell Type–Specific Loss of BDNF Signaling Mimics Optogenetic Control of Cocaine Reward

TL;DR: Examination of the roles of the two subpopulations of nucleus accumbens projection neurons in cocaine reward shows that deletion of TrkB selectively from D1+ or D2+ neurons oppositely affects cocaine reward, providing insight into the molecular control of D1- and D2-containing neuronal activity as well as the circuit-level contribution of these cell types to cocaine reward.
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