We just released the largest amount of stress profiling data from our (any?) lab so far!. How does the molecular stress response adapt as an acute stressor becomes chronic?. Multiomic profiling in the 🐭 hippocampus, led by @RebeccaWaag and co-last author Pierre-Luc Germain! 💪.

RT @SchrattL: Our study describing a role for the circular RNA circRERE in the regulation of silent excitatory synapses is finally out @Nat….

Stellar women-only (💪) panel on stress and development, loaded with cutting-edge multiomic data kicking off the European Stress Conference #ESC2025 in Innsbruck, Austria

Most importantly: We developed an automated, portable pain and welfare monitoring system (combining "mouse grimace scale" and full-body pose-estimation with behavior flow analysis). Brilliant work by @osturmscience, the @ETH_en 3R-Hub and our collaborator Katharina Hohlbaum. 💪

Note: Modest grimace pain levels remain detectable for 24hrs after surgery. Neither meloxicam (5mg/kg) nor the combination of meloxicam(5mg/kg)+buprenorphine(0.1mg/kg) could eliminate these remaining pain levels. We detect strong side-effects from opioid treatment (hyperactive).

How much analgesia is needed to manage pain levels in mice after brain surgeries?.A single dose of meloxicam seems to be enough. Even the addition of opioids cannot provide a clear benefit (in line with recent work from others, see refs in our preprint):.

And saving the best for last: We integrate these results with previously published bulk and single-cell data from our lab and make these data freely accessible and searchable through an interactive app (. We hope people like this resource - please RT! 🙏.

On a single-cell level, we reveal blunted chromatin accessibility changes after chronic stress for cAMP signaling, and a damped response that returns to baseline much faster for glucocorticoid receptor binding. This again points to two parallel mechanisms of habituation.

We replicate the profound damping of transcription on a single-cell, multi-omic level (24 biological samples), showing cell-type specificity in stress-induced transcriptional changes and diverse temporal dynamics. It seems that fewer neurons get activated.

Bioinformatic and experimental approaches identify two parallel, independent mechanisms of habituation: an early blunting of transcription due to cAMP signaling, and a late blunting related to corticosterone signaling at the glucocorticoid receptor.

We find that the transcriptional stress response dramatically habituates in every animal, profoundly blunting every stress induced gene. Habituation is already established after 10 days. There is no emergence of adaptive responses, and no change in baseline gene expression 😱!

First, we profiled the transcriptomic and chromatin accessibility response to an acute restraint stress challenge over time. Then we repeated this after 10 and 20 days of stress exposure (192 biological samples for transcriptomics, 32 for ATAC-seq).

RT @Joel_Mesot: With best wishes for 2025, I bid farewell to this communication channel. I am following various colleagues from the univers….

Opportunity of a lifetime! Join us as a professor at @ETH_en !.

RT @ETH_en: At its meeting on December 5, 2024, the ETH Board appointed nine professors at the request of ETH President Joël Mesot. In addi….

Cool! Congrats, @lustenca !.

RT @anita_luthi: @LabLuthi uncovers a dual role of #locus @coeruleus in #sleep -> 1) its strict gatekeeper role for the sleep cycle 2) the….

RT @jmourabarbosa: We did it. We killed neuro twitter and it's resuscitation it's happening somewhere else. Come join us!. .

I know I'm late to the game, but hey. @bohaceklab.bsky.social.

I have to thank the editor Nina Vogt, the editorial process was very supportive, fair and efficient. The reviewers asked for a lot, but it clearly improved the paper a lot. For a thread on the work, follow this link: