bims-adhine Biomed News
on Adult hippocampal neurogenesis
Issue of 2026–10–04
two papers selected by
Tamara J. Buijs, Universiteit van Amsterdam
  1. A ventral hippocampus-prefrontal circuit mediates the pro-extinction effects of adult hippocampal neurogenesis on contextual fear.
  2. Integrative analysis of the embryonic origin of adult neural stem cells in forebrain subventricular zones.
  1. Biol Psychiatry. 2026 Sep 28. pii: S0006-3223(26)01576-3. [Epub ahead of print]
    A ventral hippocampus-prefrontal circuit mediates the pro-extinction effects of adult hippocampal neurogenesis on contextual fear.
    Barbara Planchez, Mohamed-Lyès Kaci, Marc Legrand, Yuki Sakai, Pauline Mériau, Laurane Pena, Lea Morel, Salomé Picquet, Ambre Frerot, Bruno Brizard, Anne-Marie Le Guisquet, Eva Ploux, René Hen, Alexandre Surget, Catherine Belzung.
       BACKGROUND: Adult hippocampal neurogenesis (AHN) contributes to hippocampal functions including contextual information processing and stress responses. Inhibiting AHN increases vulnerability to stress and hinders effects of therapeutic interventions for stress-related disorders, especially post-traumatic stress disorder (PTSD) characterized by maladaptive fear response to context, suggesting that promoting AHN may offer promising strategies. We therefore aimed to test whether experimentally enhancing AHN protects against persistent contextual fear memory and examine the underlying neural circuits.
    METHODS: Using inducible Cre-dependent iBax male mice, we enhanced AHN via tamoxifen pretreatment prior to a high-intensity contextual fear conditioning (footshocks, 1.5mA, 2×2s). We assessed defensive responses to both the conditioning context and a conditioning-associated object, together with spatial memory controls, and combined retrograde labeling with projection-specific optogenetic inhibition.
    RESULTS: AHN enhancement reduced the persistence of defensive responses to fear context: accelerating within-session decline of freezing and improving next-day extinction recall, while sparing other hippocampal-dependent memory. Circuit analyses revealed increased recruitment of a ventral hippocampus-prefrontal (infralimbic) cortex pathway in AHN-enhanced mice. Critically, optogenetic inhibition of this projection did not impair extinction per se but selectively abolished the pro-extinction effects induced by AHN enhancement; an effect not reproduced by inhibiting the projection to basolateral amygdala.
    CONCLUSIONS: Ventral hippocampal input to the prefrontal cortex is not required for baseline extinction but is necessary to mediate the facilitating effects of enhanced AHN on contextual fear extinction in male mice. These findings identify a circuit mechanism through which adult neurogenesis constrains the persistence of contextual fear and promotes adaptive fear regulation.
    Keywords:  Adult neurogenesis; Contextual Fear Conditionning; Extinction; Hippocampus; Prefrontal cortex; Stress
    DOI:  https://doi.org/10.1016/j.biopsych.2026.09.017
  2. Natl Sci Rev. 2026 Sep;13(18): nwag516
    Integrative analysis of the embryonic origin of adult neural stem cells in forebrain subventricular zones.
    Huan Wu, Ke Tang, Ruimin Xu, Tao Li, Keke Liang, Xuanxuan Wang, Deyuan Huang, Yijia Yang, Yanxuan Yin, Jiayang Xie, Chong Li, Xiaoyu Liu, Qing-Ran Bai, Chenfei Wang, Qin Shen, Shaorong Gao.
      In the mammalian brain, adult neural stem cells (NSCs) located in the ventricular-subventricular zone (V-SVZ) of lateral ventricles and dentate gyrus continuously generate new neurons and glia throughout life. The adult NSCs in V-SVZ are derived from ventricular radial glial cells (RGCs) which become quiescent during embryonic development. However, the origin and establishment of this adult NSC pool remain elusive, primarily due to the challenge of tracing the lineage from embryonic RGCs to their quiescent adult successors. Here, by leveraging Vcam1-a marker continuously expressed from embryonic RGCs to adult NSCs, we unravel the dynamic process and regulatory mechanism underlying the fate bifurcation that gives rise to quiescent seed cells. We demonstrate that Vcam1+ embryonic RGCs directly contribute to the adult NSC pool. A subpopulation of quiescent Vcam1+ RGCs emerges early and is maintained throughout development, while a parallel population of proliferative Vcam1+ progenitors actively replenishes this quiescent reservoir. Through the combinatory analysis of single-cell multiomics and clonal lineage tracing of Vcam1+ cells, we identify the TGF-β/Smad3 pathway as a critical regulator of quiescence. Our work thus provides a mechanistic dissection of how the foundational adult NSC pool is established through precisely regulated fate decisions during embryogenesis, offering new insights into the principles of lifelong neurogenesis.
    Keywords:  Vcam1; adult NSCs; embryonic origin; lineage tracing; quiescence; scMulti-omics
    DOI:  https://doi.org/10.1093/nsr/nwag516
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