ArticleNature neuroscience2026
Spatiotemporal remodeling in habenula marks the onset of depression-related phenotypes.
Article in Nature neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Chronic stress has lasting adverse consequences that can lead, over time, to depression, yet the optimal timeframe for effective therapies remains unclear. The lateral habenula (LHb) has been implicated in stress-related behavioral repercussions, but the precise timing of its contribution is not understood. Here, using spatial transcriptomics, we generated a spatially resolved molecular atlas of the LHb of male mice, revealing a topographically organized and temporally defined remodeling of gene expression after chronic stress. Longitudinal in vivo two-photon calcium imaging of individual LHb neurons revealed progressively heightened excitatory responses to aversive stimuli. These neuronal adaptations mirrored both the progression of transcriptional changes and the emergence of depression-related behavioral phenotypes and were reversed by the antidepressant ketamine. Moreover, chemogenetically limiting LHb neuronal activity or administering ketamine at the onset of these changes exerted antidepressant effects. These findings link spatiotemporal signatures of LHb neuronal ensembles and genetic landscape with the onset of stress-induced depression-related states.
Identifiers
42897302What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.