One of the key features of addiction is the escalated drug intake. The neural mechanisms involved in the transition to addiction remain to be elucidated. Since abnormal neuronal activity within the subthalamic nucleus (STN) stands as potential general neuromarker common to impulse control spectrum deficits, as observed in obsessive-compulsive disorders, the present study recorded and manipulated STN neuronal activity during the initial transition to addiction (i.e., escalation) and post-abstinence relapse (i.e., re-escalation) in rats with extended drug access. We found that low-frequency (theta and beta bands) neuronal oscillations in the STN increase with escalation of cocaine intake and that either lesion or high-frequency stimulation prevents the escalation of cocaine intake. STN-HFS also reduces re-escalation after prolonged, but not short, protracted abstinence, suggesting that STN-HFS is an effective prevention for relapse when baseline rates of self-administration have been re-established. Thus, STN dysfunctions may represent an underlying mechanism for cocaine addiction and therefore a promising target for the treatment of addiction.
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Effects of STN lesions on simple vs choice reaction time tasks in the rat: preserved motor readiness, but impaired response selection
Dopamine regulates the impact of the cerebral cortex on the subthalamic nucleus-globus pallidus network
High frequency stimulation of the subthalamic nucleus has beneficial antiparkinsonian effects on motor functions in rats, but less efficiency in a choice reaction time task
Effects of extended access to high versus low cocaine doses on self-administration, cocaine-induced reinstatement and brain mRNA levels in rats
Sex differences in the escalation of intravenous cocaine intake following long- or short-access to cocaine self-administration
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Alpha 1-noradrenergic system role in increased motivation for cocaine intake in rats with prolonged access
Disrupted dopamine transmission and the emergence of exaggerated beta oscillations in subthalamic nucleus and cerebral cortex
Deep brain stimulation of the nucleus accumbens shell attenuates cocaine priming-induced reinstatement of drug seeking in rats
Is there an inhibitory-response-control system in the rat? Evidence from anatomical and pharmacological studies of behavioral inhibition
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Different populations of subthalamic neurons encode cocaine vs. sucrose reward and predict future error
Escalation of cocaine intake and incubation of cocaine seeking are correlated with dissociable neuronal processes in different accumbens subregions
Oscillatory subthalamic nucleus activity is modulated by dopamine during emotional processing in Parkinson's disease
Addiction therapy. Refining deep brain stimulation to emulate optogenetic treatment of synaptic pathology
Subthalamic nucleus activity in the awake hemiparkinsonian rat: relationships with motor and cognitive networks
Subthalamic nucleus high-frequency stimulation modulates neuronal reactivity to cocaine within the reward circuit
The human subthalamic nucleus encodes the subjective value of reward and the cost of effort during decision-making
Subthalamic, not striatal, activity correlates with basal ganglia downstream activity in normal and parkinsonian monkeys
High-Frequency Stimulation of the Subthalamic Nucleus Blocks Compulsive-Like Re-Escalation of Heroin Taking in Rats
Deep-Brain Stimulation of the Subthalamic Nucleus Selectively Decreases Risky Choice in Risk-Preferring Rats
Opposite environmental gating of the experienced utility ('liking') and decision utility ('wanting') of heroin versus cocaine in animals and humans: implications for computational neuroscience
Shifts in the neurobiological mechanisms motivating cocaine use with the development of an addiction-like phenotype in male rats.
Deep Brain Stimulation of the Subthalamic Nucleus Modulates Reward-Related Behavior: A Systematic Review
In vivo validation of a new portable stimulator for chronic deep brain stimulation in freely moving rats
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