Нейрохимия, Год журнала: 2024, Номер 41(3), С. 231 - 239
Опубликована: Ноя. 28, 2024
Язык: Английский
Science, Год журнала: 2024, Номер 385(6713), С. 1081 - 1086
Опубликована: Сен. 5, 2024
Negative emotional contagion-witnessing others in distress-affects an individual's responsivity. However, whether it shapes coping strategies when facing future threats remains unknown. We found that mice briefly observe a conspecific being harmed become resilient, withstanding behavioral despair after adverse experience. Photometric recordings during negative contagion revealed increased serotonin (5-HT) release the lateral habenula. Whereas 5-HT and reduced habenular burst firing, limiting synthesis prevented plasticity. Enhancing raphe-to-habenula was sufficient to recapitulate resilience. In contrast, reducing habenula made witnessing distress ineffective promote resilient phenotype adversity. These findings reveal supports vicarious emotions leads resilience by tuning definite patterns of neuronal activity.
Язык: Английский
Процитировано
8
Immunity, Год журнала: 2025, Номер 58(1), С. 10 - 12
Опубликована: Янв. 1, 2025
Язык: Английский
Процитировано
0
Neuroscience Research, Год журнала: 2025, Номер unknown
Опубликована: Фев. 1, 2025
Язык: Английский
Процитировано
0
Nature Communications, Год журнала: 2025, Номер 16(1)
Опубликована: Март 8, 2025
Early life experience modulates resilience to stress in later life. Previous research implicated maternal care as a key mediator of behavioral responses the adversity adolescence, but details molecular mechanisms remain elusive. Here, we show social activates transcription factor C/EBPβ mPFC neurons adolescent mice, which transcriptionally upregulates Dnm1l and promotes mitochondrial dysfunction, thereby conferring susceptibility mice. Moreover, different separation differentially regulates susceptibility. Mechanistically, this differential effect depends on behavior-stimulated IGF-1, inhibits neuronal through mTORC1-induced C/EBPβ-LIP translation. Furthermore, identify IGF-1 is mainly released from microglia. Notably, increased under an environmental enrichment condition or behavior impairment induced by repeated MPOAEsr1+ cells inhibition dams prevents via microglial-to-neuronal IGF-1-C/EBPβ-DRP1 signaling. In work, these findings have unveiled adolescents. Here authors that triggers microglia-derived levels, suppresses C/EBPβ-DRP1 axis, promoting
Язык: Английский
Процитировано
0
Neuron, Год журнала: 2025, Номер unknown
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0
Frontiers in Neural Circuits, Год журнала: 2025, Номер 19
Опубликована: Март 26, 2025
The prefrontal cortex (PFC), located at the anterior region of cerebral cortex, is a multimodal association essential for higher-order brain functions, including decision-making, attentional control, memory processing, and regulation social behavior. Structural, circuit-level, functional abnormalities in PFC are often associated with neurodevelopmental disorders. Here, we review recent findings on postnatal development PFC, particular emphasis rodent studies, to elucidate how its structural circuit properties established during critical developmental windows these processes influence adult behaviors. Recent evidence also highlights lasting effects early life stress structure, connectivity, function. We explore potential mechanisms underlying stress-induced alterations, focus epigenetic implications maturation By integrating insights, this provides an overview shaping their health disease.
Язык: Английский
Процитировано
0
Brain Research Bulletin, Год журнала: 2025, Номер 225, С. 111335 - 111335
Опубликована: Апрель 8, 2025
The pathogenesis of depression is fundamentally linked to the dysregulation neural circuit structure and function. Notably, medial prefrontal cortex (mPFC) basolateral amygdala (BLA) are critical brain regions in regulation depression-related behaviors. Depressed rats exhibited attenuated messaging between mPFC BLA, along with abnormally enhanced theta oscillations BLA during execution an exploratory task. However, whether specific activation improves behavior recovery mediated by mPFC-BLA circuitry unknown. We modeled using chronic unpredictable mild stimulation (CUMS) employed chemogenetic approaches selectively activate glutamatergic neurons depressed rats. Through simultaneous monitoring behavioral patterns local field potentials (LFPs) both open-field exploration, we conducted comparative analyses chemogenetically activated sham-stimulated groups. Our investigation focused on oscillation dynamics, network connectivity strength, interregional information transfer behavior. results demonstrated that not only ameliorated deficits but also mPFC-to-BLA while attenuating oscillations. These findings suggest restoration flow may play a crucial role improving behavior, thereby revealing potential mechanism underlying depressive state modulation.
Язык: Английский
Процитировано
0
Biological Psychiatry, Год журнала: 2025, Номер 97(9), С. 844 - 846
Опубликована: Апрель 9, 2025
Язык: Английский
Процитировано
0
International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(8), С. 3517 - 3517
Опубликована: Апрель 9, 2025
Stress-induced demyelination resulting from oligodendrocyte (OLG) dysfunction is one of the key pathological mechanisms depression, yet its dynamic regulatory network remains unclear. This study integrates single-cell transcriptomics, lineage tracing, and functional interventions to uncover a temporally disordered OLG cholesterol metabolism in restraint stress mouse model: After 3 days stress, upregulation efflux genes Abca1/Abcg1 triggers compensatory response; however, by day 14, persistent suppression transport (Apoe, Apod) homeostatic (Dhcr24, Srebf2, etc.) leads intracellular accumulation “ineffective cholesterol”, with activation AMPK pathway unable restore conversion into myelin. Pseudotime analysis further reveals that alters differentiation trajectories, decreasing proportion mature OLGs causing immature precursors abnormally stall at late pre-differentiation stage, myelin regeneration failure. Moreover, an immune OLG_C10 subpopulation expressing complement component C3 P2ry12 identified, indicating may contribute neuroinflammatory cascades through reprogramming. In summary, these findings reveal novel mechanism perspective OLGs, which interplay “metabolic imbalance, blockade, activation” collaboratively drives stress-induced demyelination, providing theoretical foundation for depression treatment targeting restoration.
Язык: Английский
Процитировано
0
Nature, Год журнала: 2025, Номер unknown
Опубликована: Апрель 9, 2025
Язык: Английский
Процитировано
0