Repeated cocaine reorganizes striatal ensembles along the ventral-dorsal axis
Leonard, M. Z.; Reiley, H. B.; Konomi Pilkati, A.; Bjornson, K. J.; Chevee, M. F.; Calipari, E. S.
Show abstract
Drugs of abuse produce lasting adaptations in the striatum. A prominent theory holds that the early reinforcing effects of cocaine preferentially engage the ventral striatum, and repeated cocaine use recruits dorsal striatal systems associated with habitual drug-related behavior. However, this transition has largely been conceptualized on the population level, obscuring how it is implemented within individual neurons and how repeated drug exposure reorganizes drug responsivity within these circuits. Here, we used single-cell calcium imaging to examine ventral and dorsal striatal responses to acute and repeated cocaine exposure in mice. Cocaine broadly suppressed neuronal activity throughout the ventral and dorsal striatum. However, repeated exposure produced opposing changes in cocaine-modulated neurons across the ventral-dorsal axis. The cocaine-activated population was reduced ventrally while expanding dorsally. Unique to dorsal striatum, repeated cocaine engendered two distinct features of activity: 1) Cocaine-activated cells had weak baseline coupling with the surrounding neuronal population and 2) The emergence of a subpopulation of neurons exhibiting regular, slow rhythmic activity in response to cocaine. Thus, repeated cocaine effects reflect a change in how the circuit is organized rather than simply how strongly it is engaged. This organization may allow cocaine to engage patterns of dorsal striatal activity that are largely absent under baseline conditions, creating a circuit state that becomes increasingly specific to the presence of the drug.
Matching journals
The top 5 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Dopamine transmission at D1 and D2 receptors in the nucleus accumbens contributes to the expression of incubation of cocaine craving 94%
- Dorsal Raphe to Basolateral Amygdala Corticotropin-Releasing Factor Circuit Regulates Cocaine-Memory Reconsolidation 94%
- Risky Decision-Making Predicts Dopamine Release Dynamics in Nucleus Accumbens Shell 94%
Similar papers in this journal
- Prior cocaine exposure increases firing to immediate reward while attenuating cue and context signals related to reward value in anterior insula 95%
- The mesolimbic dopamine signatures of relapse to alcohol-seeking 94%
- Dopamine release in nucleus accumbens is under tonic inhibition by adenosine A1 receptors regulated by astrocytic ENT1 and dysregulated by ethanol 93%
Similar papers in this journal
- Epac2 in midbrain dopamine neurons contributes to cocaine reinforcement via facilitation of dopamine release 94%
- Dynamic dichotomy of accumbal population activity underlies cocaine sensitization 94%
- Dopamine in the Dorsal Bed Nucleus of Stria Terminalis signals Pavlovian sign-tracking and reward violations 94%
Similar papers in this journal
- Accumbens cholinergic interneurons mediate cue-induced nicotine seeking and associated glutamatergic plasticity 92%
- The role of genetically distinct central amygdala neurons in appetitive and aversive responding assayed with a novel dual valence operant conditioning paradigm. 91%
- Dopamine and calcium dynamics in the nucleus accumbens core during food seeking 91%
Similar papers in this journal
- Drug Reinforcement Impairs Cognitive Flexibility by Inhibiting Striatal Cholinergic Neurons 94%
- Noradrenergic alpha-2a Receptor Stimulation Enhances Prediction Error Signaling in Anterior Cingulate Cortex and Striatum 93%
- Plasticity in striatal dopamine release is governed by release-independent depression and the dopamine transporter 92%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.