Those with cocaine use disorder who were administered ketamine for depression or pain experienced two-to-four times higher remission rate.
Cocaine use supports the growth of γ-proteobacteria, a common gut bacteria that consume glycine. As glycine levels become depleted mouse models exhibit a higher response to cocaine with abnormal behaviors including increased drug-induced locomotion and drug-seeking behaviors.
Greater impairment of the prefrontal cortex-habenula pathway was correlated with earlier age of first drug use.
Blocking M2Rs muscarinic acetylcholine receptors in the lateral habenula with an experimental drug increased cocaine-seeking behaviors in rat models of impulsive behaviors.
Mouse study reveals sleep deprivation can increase the risk of cocaine addiction. Too little sleep increases the reward properties of cocaine, researchers report.
Cocaine and sucrose neuron ensembles in the nucleus accumbens are mostly non-overlapping.
Astrocytes respond to cocaine exposure in the brains of mice by promoting the formation of new synapses.
A new study reveals the role the claustrum plays in cocaine addiction. Inhibiting claustral neurons prevented behavioral responses to cocaine in mouse models of addiction.
Reducing H3Q5dop in rat models of cocaine withdrawal significantly reversed cocaine mediated gene expression changes and reduced cocaine-seeking behaviors.
In men with a history of childhood trauma, oxytocin reduced the activity within the amygdala and cravings for cocaine. Women who were addicted to cocaine and had experienced childhood trauma showed an increase in amygdala activity following exposure to oxytocin.
Chronic cocaine use alters the epigenetic profile of the FosB gene in the hippocampus. These alterations are required for cocaine-dependent gene expression and cocaine environment associations. Modification of hippocampal FosB results in a condition critical for cocaine-related learning.
Teens who use anabolic steroids are at increased risk of cocaine use disorder, researchers report.
