2025/08/05 by Hermina Nedelescu, Elias Meamari, Nami Rajaei +5 · 1 voice
Neuroscience · Psychology · #Neurotransmitter Receptor Influence on Behavior #Obsessive-Compulsive Spectrum Disorders #Memory and Neural Mechanisms
paper · doi:10.1016/j.bpsgos.2025.100578
openalex publication_date 2025/08/05 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/01
ABSTRACT Background Stimulus-reactive neuronal populations are groups of neurons that become activated by environmental stimuli. These sparsely activated neuronal assemblies are implicated in encoding associations between environmental contexts and subjectively rewarding or aversive experiences that regulate behavior. How positive- or negative-hedonic states are represented in brain neurocircuits is a fundamental question relevant for understanding the processing of emotionally meaningful stimuli that drive appropriate vs. maladaptive behavior. It is well-known that animals avoid noxious stimuli and experiences. Little is known, however, how the conditioning of environmental stimuli to behavior that leads to amelioration of dysphoric states establishes powerful associations that lead to compulsive maladaptive behavior. Methods Here we sought to identify stimulus-reactive neurons that may mediate the conditioned effects of environmental stimuli associated with the reversal of dysphoric alcohol withdrawal states using a dependent withdrawal-related (WDL) experimental condition (DEP-WDL, N=13) and three controls: NDEP-WDL (N=12), DEP-NWDL (N=9), NDEP-NWDL (N=9). Results The results document a role for clusters of neurons in the paraventricular nucleus of the thalamus (PVT, n=8), the central nucleus of the amygdala (CeA, n=8), and the dorsal striatum (DS, n=9) in this conditioned negative reinforcement process. Conclusions These findings suggest that associations between reversal of negative hedonic states and environmental contexts are encoded in distinct neuronal populations which may serve as a neural substrate of compulsive alcohol seeking and vulnerability to relapse associated with reward dysregulation and hedonic allostasis.