Jeremy Day
@daylab.bsky.social
2.1K followers 580 following 170 posts
Neuroscientist at UAB interested in molecular and genetic mechanisms in brain function. Director, UAB Comprehensive Neuroscience Center.
Posts Media Videos Starter Packs
daylab.bsky.social
Congratulations Ishmail - incredibly well deserved! I'm excited to follow the many fundamental questions you will be able to answer with this research program!
Reposted by Jeremy Day
ishmailsaboor.bsky.social
I’m extremely honored to be a recipient of the NIH Director’s Pioneer Award!
zuckermanbrain.bsky.social
Congratulations to @ishmailsaboor.bsky.social on receiving the NIH Director’s Pioneer Award, celebrating “scientists with outstanding records of creativity.” His lab will explore how the sense of touch can help build relationships. 🫶🧠💡

See zuckermaninstitute.columbia.edu/zuckerman-in...
Ishmail Abdus-Saboor
daylab.bsky.social
Congratulations Beth! We are so happy to have you at UAB, and this is a well deserved honor!
daylab.bsky.social
Very cool work David! Interesting that opioids produce rewarding effects at doses that are 30 times lower than the doses required to produce analgesic effects. These kinds of careful dose response studies are incredibly useful to the entire field!
daylab.bsky.social
Thanks David! I hope it is useful - we have made the object available on Zenodo but let me know if there is anything specific you'd like to know about the dataset!
daylab.bsky.social
As always, data for this manuscript will be freely available at www.ratlas.org or via direct download (please see GEO accession number of Zenodo links in preprint).
Ratlas
ratlas.org
daylab.bsky.social
Collectively, these findings reveal that glial cells within reward circuits undergo profound transcriptional responses to opioids through indirect, stress-hormone mediated mechanisms, highlighting a previously unappreciated non-neuronal contribution to opioid-induced neural adaptations.
daylab.bsky.social
A final note, buried in a supplemental figure but still very cool. The main place we saw interactions between pain and opioid exposure was in astrocytes as well. Here, pain states often created gene expression changes that were rescued by morphine administration!
daylab.bsky.social
Next, we generated an astrocyte-targeted CRISPR tool to allow us to knock down NR3C1 in this population, and found that this also completely blocked the ability of cortisol to induce FKBP5.
daylab.bsky.social
Application of cortisol onto these cells robustly increased FKBP5 levels, and this effect could be blocked by pretreatment with the glucocorticoid receptor antagonist mifepristone. We observed no changes when cells were treated with the µOR agonist DAMGO.
daylab.bsky.social
To test this directly, we generated a human-derived astrocyte model from cells with a ventral midbrain origin. As you can see here, they are beautiful and express known astrocyte marker genes like GFAP and S100B.
daylab.bsky.social
Since glial populations also exhibited elevated expression of Nr3c1, a gene encoding the glucocorticoid receptor, we suspected that these glial changes may be driven by the well-known ability of opioids to increase cortisol/corticosterone.
daylab.bsky.social
Among the genes that was strongly induced in glial populations was Fkbp5, a co-chaperone closely linked to glucocorticoid signaling and stress response. Transcripts from this gene were increased in astrocytes, microglia, and oligodendrocytes, but not neurons.
daylab.bsky.social
However, to our surprise, the largest effects of opioids and pain/opioid interactions were observed in glial cells, such as astrocytes and oligodendrocytes, despite a lack of µOR expression in these cells.
daylab.bsky.social
Consistent with this model, we found enriched expression of Oprm1, the gene that encodes the µOR, in a select population of GABA neurons. Additionally, we report selective increases in immediate early genes in dopamine neurons after morphine administration.
daylab.bsky.social
A classic circuit model for the rewarding effects of opioids posits that they decrease inhibition onto dopamine neurons by silencing GABAergic neurons that express the mu opioid receptor (µOR), the primary receptor target of commonly used opioids.
daylab.bsky.social
We focused on the ventral tegmental area (VTA), a key brain reward region that includes dopamine neurons which project to forebrain structures. The rat VTA is complex - we find multiple types of dopamine, glutamate, and GABA neurons, as well as various glial cell classes.
daylab.bsky.social
Excited to share this new work from the lab, in collaboration with @jtuscher.bsky.social & Rob Sorge! Here, we used single cell transcriptional profiling to define molecular adaptations induced by chronic pain and opioid experience, which often occur in conjunction.

www.biorxiv.org/content/10.1...
daylab.bsky.social
What a great retreat! Thanks to the entire UAB neuroscience community for contributing their science, and to @ishmailsaboor.bsky.social for an awesome keynote lecture!
uabneuro.bsky.social
The 2025 CNC Retreat is in the books! 📖 Thank you to the 220+ attendees for being a part of this annual event and making it a grand success. More photos coming soon. 😎
daylab.bsky.social
One of my favorite events that we @uabneuro.bsky.social host each year, and excited to have @ishmailsaboor.bsky.social here for the keynote!
uabneuro.bsky.social
The annual UAB CNC retreat starts tomorrow in our beautiful new Heersink Institute for Biomedical Innovation Conference Center! Join us for trainee and faculty science as well as a keynote presentation from @ishmailsaboor.bsky.social! Link to program below.
www.uab.edu/medicine/cnc...
daylab.bsky.social
Excited to be co-chairing this @acnporg.bsky.social panel with chair @kr-maynard.bsky.social on opioid-responsive subpopulations in brain reward circuits. Special thanks to @rphillips3.bsky.social for helping to assemble the panel!