Role of ventral subiculum neuronal ensembles in incubation of oxycodone craving after electric barrier-induced voluntary abstinence.
Ida FredrikssonPei-Jung TsaiAniruddha ShekaraYing DuanSarah V ApplebeyAngélica Minier-ToribioAshley BatistaJonathan J ChowLindsay AltidorEstelle BarbierCarlo CifaniXuan LiDavid J ReinerF Javier RubioBruce T HopeYihong YangJennifer M BossertYavin ShahamPublished in: Science advances (2023)
High relapse rate is a key feature of opioid addiction. In humans, abstinence is often voluntary due to negative consequences of opioid seeking. To mimic this human condition, we recently introduced a rat model of incubation of oxycodone craving after electric barrier-induced voluntary abstinence. Incubation of drug craving refers to time-dependent increases in drug seeking after cessation of drug self-administration. Here, we used the activity marker Fos, muscimol-baclofen (GABAa + GABAb receptor agonists) global inactivation, Daun02-selective inactivation of putative relapse-associated neuronal ensembles, and fluorescence-activated cell sorting of Fos-positive cells and quantitative polymerase chain reaction to demonstrate a key role of vSub neuronal ensembles in incubation of oxycodone craving after voluntary abstinence, but not homecage forced abstinence. We also used a longitudinal functional magnetic resonance imaging method and showed that functional connectivity changes in vSub-related circuits predict opioid relapse after abstinence induced by adverse consequences of opioid seeking.
Keyphrases
- smoking cessation
- chronic pain
- functional connectivity
- pain management
- magnetic resonance imaging
- drug induced
- resting state
- high glucose
- mental health
- endothelial cells
- adverse drug
- free survival
- diabetic rats
- single cell
- spinal cord
- cerebral ischemia
- computed tomography
- machine learning
- magnetic resonance
- stem cells
- cell cycle arrest
- high resolution
- mass spectrometry
- cell proliferation
- blood brain barrier
- bone marrow
- deep learning
- subarachnoid hemorrhage
- endoplasmic reticulum stress