ORCID Profile
0000-0002-9607-4228
Current Organisation
UNSW Sydney
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Publisher: Society for Neuroscience
Date: 27-10-2018
DOI: 10.1523/JNEUROSCI.2460-17.2017
Abstract: BLA neurons serve a well-accepted role in fear conditioning and fear extinction. However, the specific learning processes related to their activity at different times during learning remain poorly understood. We addressed this using behavioral tasks isolating distinct aspects of fear learning in male rats. We show that brief optogenetic inhibition of BLA neurons around moments of aversive reinforcement or nonreinforcement causes reductions in the salience of conditioned stimuli, rendering these stimuli less able to be learned about and less able to control fear or safety behaviors. This salience reduction was stimulus-specific, long-lasting, and specific to learning about, or responding to, the same aversive outcome, precisely the goals of therapeutic interventions in human anxiety disorders. Our findings identify a core learning process disrupted by brief BLA optogenetic inhibition. They show that a primary function of the unconditioned stimulus-evoked activity of BLA neurons is to maintain the salience of conditioned stimuli that precede it. This maintenance of salience is a necessary precursor for these stimuli to gain and maintain control over fear and safety behavior. SIGNIFICANCE STATEMENT The amygdala is essential for learning to fear and learning to reduce fear. However, the specific roles served by activity of different amygdala neurons at different times during learning is poorly understood. We used behavioral tasks isolating distinct aspects of learning in rats to show that brief optogenetic inhibition of BLA neurons around moments of reinforcement or nonreinforcement disrupts maintenance of conditioned stimulus salience. This causes a stimulus-specific and long-lasting deficit in the ability of the conditioned stimulus to be learned about or control fear responses. These consequences are the precisely goals of therapeutic interventions in human anxiety disorders. Our findings identify a core learning process disrupted by brief BLA optogenetic inhibition.
Publisher: Society for Neuroscience
Date: 15-07-2020
Publisher: Wiley
Date: 10-02-2021
DOI: 10.1111/JNC.15309
Abstract: The actions of dopamine are essential to relapse to drug seeking but we still lack a precise understanding of how dopamine achieves these effects. Here we review recent advances from animal models in understanding how dopamine controls relapse to drug seeking. These advances have been enabled by important developments in understanding the basic neurochemical, molecular, anatomical, physiological and functional properties of the major dopamine pathways in the mammalian brain. The literature shows that although different forms of relapse to seeking different drugs of abuse each depend on dopamine, there are distinct dopamine mechanisms for relapse. Different circuit‐level mechanisms, different populations of dopamine neurons and different activity profiles within these dopamine neurons, are important for driving different forms of relapse. This ersity highlights the need to better understand when, where and how dopamine contributes to relapse behaviours. image
Publisher: Elsevier BV
Date: 05-2018
DOI: 10.1016/J.NEURON.2018.03.033
Abstract: Contexts exert bi-directional control over relapse to drug seeking. Contexts associated with drug self-administration promote relapse, whereas contexts associated with the absence of self-administration protect against relapse. The nucleus accumbens shell (AcbSh) is a key brain region determining these roles of context. However, the specific cell types, and projections, by which AcbSh serves these dual roles are unknown. Here, we show that contextual control over relapse and abstinence is embedded within distinct output circuits of dopamine 1 receptor (Drd1) expressing AcbSh neurons. We report anatomical and functional segregation of Drd1 AcbSh output pathways during context-induced reinstatement and extinction of alcohol seeking. The AcbSh→ventral tegmental area (VTA) pathway promotes relapse via projections to VTA Gad1 neurons. The AcbSh→lateral hypothalamus (LH) pathway promotes extinction via projections to LH Gad1 neurons. Targeting these opposing AcbSh circuit contributions may reduce propensity to relapse to, and promote abstinence from, drug use.
No related grants have been discovered for Yu Liu.