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Cross‐sensitization between cocaine and acute restraint stress is associated with sensitized dopamine but not glutamate release in the nucleus accumbens
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The 71 checked references that resolve
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Effects of tissue trauma on the characteristics of microdialysis zero-net-flux method sampling neurotransmitters
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Repeated Cocaine Alters Glutamate Receptor Subunit Levels in the Nucleus Accumbens and Ventral Tegmental Area of Rats that Develop Behavioral Sensitization
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Central administration of a CRF antagonist blocks the development of stress-induced behavioral sensitization
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Stress at Learning Facilitates Memory Formation by Regulating AMPA Receptor Trafficking Through a Glucocorticoid Action
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Phosphorylation-Dependent Trafficking of GluR2-Containing AMPA Receptors in the Nucleus Accumbens Plays a Critical Role in the Reinstatement of Cocaine Seeking
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The stress hormone corticosterone conditions AMPAR surface trafficking and synaptic potentiation
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Extinction Training after Cocaine Self-Administration Induces Glutamatergic Plasticity to Inhibit Cocaine Seeking
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Cocaine Experience Controls Bidirectional Synaptic Plasticity in the Nucleus Accumbens
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Glutamate Release in the Nucleus Accumbens Core Is Necessary for Heroin Seeking
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Interaction between glucocorticoid hormones, stress and psychostimulant drugs*
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Corticosterone Alters AMPAR Mobility and Facilitates Bidirectional Synaptic Plasticity
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Prefrontal Glutamate Release into the Core of the Nucleus Accumbens Mediates Cocaine-Induced Reinstatement of Drug-Seeking Behavior
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Limbic and Motor Circuitry Underlying Footshock-Induced Reinstatement of Cocaine-Seeking Behavior
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Reversing cocaine-induced synaptic potentiation provides enduring protection from relapse
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The Flexible Approach Hypothesis: Unification of Effort and Cue-Responding Hypotheses for the Role of Nucleus Accumbens Dopamine in the Activation of Reward-Seeking Behavior
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A Glutamate–Dopamine Interaction in the Persistent Enhanced Response to Amphetamine in Nucleus Accumbens Core but not Shell Following a Single Restraint Stress
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Computational model of extracellular glutamate in the nucleus accumbens incorporates neuroadaptations by chronic cocaine
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Amphetamine produces sensitized increases in locomotion and extracellular dopamine preferentially in the nucleus accumbens shell of rats administered repeated cocaine.
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Repeated cocaine augments excitatory amino acid transmission in the nucleus accumbens only in rats having developed behavioral sensitization
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Individual differences in stress‐induced dopamine release in the nucleus accumbens are influenced by corticosterone
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Drugs of Abuse and Stress Trigger a Common Synaptic Adaptation in Dopamine Neurons
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Prolonged Withdrawal from Repeated Noncontingent Cocaine Exposure Increases NMDA Receptor Expression and ERK Activity in the Nucleus Accumbens
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Previous Exposure to Psychostimulants Enhances the Reinstatement of Cocaine Seeking by Nucleus Accumbens AMPA
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Extracellular fluctuations of dopamine and glutamate in the nucleus accumbens core and shell associated with lever-pressing during cocaine self-administration, extinction, and yoked cocaine administration
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Corticotropin-Releasing Factor Requires CRF Binding Protein to Potentiate NMDA Receptors via CRF Receptor 2 in Dopamine Neurons
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Sensitization of Midbrain Dopamine Neuron Reactivity Promotes the Pursuit of Amphetamine
resolves10.1113/jphysiol.2007.150078
Corticotropin‐releasing factor increases mouse ventral tegmental area dopamine neuron firing through a protein kinase C‐dependent enhancement of<i>I</i><sub>h</sub>
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Cocaine Experience Establishes Control of Midbrain Glutamate and Dopamine by Corticotropin-Releasing Factor: A Role in Stress-Induced Relapse to Drug Seeking
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Stress-induced relapse to cocaine seeking: roles for the CRF2 receptor and CRF-binding protein in the ventral tegmental area of the rat
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Stress and rodent models of drug addiction: role of VTA–accumbens–PFC–amygdala circuit
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