Neuropharmacology, Год журнала: 2024, Номер unknown, С. 110264 - 110264
Опубликована: Дек. 1, 2024
Язык: Английский
Neuropharmacology, Год журнала: 2024, Номер unknown, С. 110264 - 110264
Опубликована: Дек. 1, 2024
Язык: Английский
Neuron, Год журнала: 2025, Номер unknown
Опубликована: Май 1, 2025
Язык: Английский
Процитировано
1Neuropharmacology, Год журнала: 2025, Номер unknown, С. 110371 - 110371
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
0Cell Reports, Год журнала: 2025, Номер 44(4), С. 115482 - 115482
Опубликована: Март 29, 2025
Язык: Английский
Процитировано
0EBioMedicine, Год журнала: 2025, Номер 115, С. 105684 - 105684
Опубликована: Апрель 17, 2025
Язык: Английский
Процитировано
0Research Square (Research Square), Год журнала: 2025, Номер unknown
Опубликована: Май 9, 2025
The infralimbic (IL) subregion of the prefrontal cortex (PFC), via its descending projection to nucleus accumbens (NAc), inhibits cue-induced drug seeking and reinstatement, but underlying mechanisms are not fully understood. Here we show that activity IL layer 5 pyramidal neurons projecting NAc shell (IL-NAcSh neurons) suppresses cocaine-associated memories. Following repeated cocaine exposures in a conditioned place preference paradigm, IL-NAcSh anatomically traced by fluorescent Retrobeads undergo prolonged decrease membrane excitability, lasting for at least 15 days after withdrawal. This persistent neuron hypoexcitability is accompanied an increase rheobase, afterhyperpolarization potential, input resistance. induced neuroadapation intrinsic excitability observed prelimibic core (PL-NAcCo neurons), separate circuit thought promote cue-triggered seeking. Chemogenetic restoration extinguishes both acquisition retention Our results provide direct support notion serves extinct associated memories restoring impaired has potential mitigate drug-cue association
Язык: Английский
Процитировано
0bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown
Опубликована: Авг. 6, 2024
SUMMARY Adaptive regulation of feeding depends on linkage internal states and food outcomes with contextual cues. Human brain imaging has identified dysregulation a hippocampal-lateral hypothalamic area (LHA) network in binge eating, but mechanistic instantiation underlying cell-types circuitry is lacking. Here, we identify an evolutionary conserved discrete Prodynorphin ( Pdyn )-expressing subpopulation Somatostatin Sst inhibitory neurons the dorsolateral septum (DLS) that receives primarily dorsal, not ventral, hippocampal inputs. DLS( ) inhibit LHA GABAergic confer context- state-dependent calibration feeding. Viral deletion DLS mimicked effects seen optogenetic silencing INs, suggesting potential role for DYNORPHIN-KAPPA OPIOID RECEPTOR signaling food-seeking. Together, our findings illustrate how dorsal hippocampus evolved to recruit ancient circuit module through link information consumption. HIGHLIGHTS receive dense input from ventral Silencing hippocampus-DLS( )-LHA nodes abolishes context-conditioned necessary
Язык: Английский
Процитировано
1Neuroscience Research, Год журнала: 2024, Номер unknown
Опубликована: Сен. 1, 2024
Язык: Английский
Процитировано
1Cell Reports, Год журнала: 2024, Номер 43(12), С. 115074 - 115074
Опубликована: Дек. 1, 2024
The association between drug-induced rewards and environmental cues represents a promising strategy to address addiction. However, the neural networks molecular mechanisms orchestrating methamphetamine (MA)-associated memories remain incompletely characterized. In this study, we demonstrated that AdipoRon (AR), specific adiponectin receptor (AdipoR) agonist, inhibits formation of MA-induced conditioned place preference (CPP) in MA-conditioned mice, accompanied by suppression basolateral amygdala (BLA) CaMKIIα neuron activity. Furthermore, identified an excitatory circuit from BLA prelimbic cortex (PrL) integration with cues. We also determined phosphorylated AMPK (p-AMPK)/Cav1.3 signaling pathway mediates modulatory effects AdipoR1 PrL-projecting neurons on MA reward memories, process influenced physical exercise. These findings highlight critical function
Язык: Английский
Процитировано
1bioRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown
Опубликована: Авг. 13, 2024
SUMMARY Rapid escape against visual threats is critical for survival. Whether it requires a permissive mechanism unknown. Here, we show that osteocalcin (OCN), protein produced by bone and persisted in the brain, primes rapid response increasing excitability of VTA GABAergic neuron subpopulation via OCN-GPR37-cAMP-THIK-1 (K 2P 13.1) pathway. Knock-out OCN or its receptor GPR37, conditional knock-out GPR37 glutamatergic neurons caused delayed escape. Reconstituting OCN-GPR37 signaling specifically was sufficient to restore normal response. Single-cell transcriptomics combined with electrophysiology showed decreases potassium currents GPR37-induced cAMP reduction subsequent THIK-1 suppression. This elevation can be recapitulated HM4Di, an inhibitory chemogenetic GPCR commonly used suppress neuronal activity. Our study demonstrated behavior bone-derived tunes central nervous system neurons. Graph Abstract In brief The bone-brain axis regulates behavior. Osteocalcin small secreted bone, plays role achieved through expressed increases decreasing K+ current channel Highlights are required Osteocalcin-GPR37 suppressing reduction. Activation HM4Di enhances
Язык: Английский
Процитировано
0Neuron, Год журнала: 2024, Номер 112(16), С. 2666 - 2668
Опубликована: Авг. 1, 2024
Язык: Английский
Процитировано
0