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Mugshot aka our-hair-looks-so-good-from-behind (
@beebosity)pic.twitter.com/KM3Gy3cPud
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These are from P5-P7 mice - you can tell because the Purkinje cells are still stubby and the granule cells haven't finished migrating down to the granule cell layer.
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I was looking through my old immuno images for a pretty picture to use as my lab meeting title slide and happened across these psychedelic images of developmental timepoints.pic.twitter.com/BHtLLy35w8
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When I try to read papers at home in the evening I fall asleep but when I try to code in the evening I completely lose track of time and could stay up forever!
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I’m at that point in my PhD when I bring two travel mugs of coffee to work on days I know I’m going to be reading/analyzing/coding all day.
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Hvala. Twitter će to iskoristiti za poboljšanje vaše vremenske crte. PoništiPoništi
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I spent my free time learning cross-stitch via this tiny donut Pusheen.pic.twitter.com/MibsVQzGE0
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Snowy weekend getaway: no internet, no cell service, surround by nature but with running water and heat.pic.twitter.com/aCElegnqQM
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A lot of really stellar scientists worked on this project, none of which are on twitter. So, shoutout to Ivar Stein (postdoc turned project scientist), Deborah Park (phys/pharm graduate student), Juan Flores (mol/cell graduate student), and our PI: Karen Zito!
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Indeed, we found that CaMKII, nNOS, NOS1AP, p38 MAPK, MK2, and cofilin were all necessary for non-ionotropic spine shrinkage.pic.twitter.com/o7EXD5un0g
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Our paper uses 2-photon glutamate uncaging to induce LTP at single spines. This results in reduced synaptic strength (assayed with ephys) and spine shrinkage. We then blocked potential signaling molecules and looked to see if this also blocked spine shrinkage.
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Before our paper, the only known players in the non-ionotropic signaling pathway were p38 MAPK, CaMKII, and PP2A. Here we parse out the signaling pathway, linking NMDA receptor agonism and the associated conformational change to AMPA receptor endocytosis.
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But people didn't like calling it metabotropic because NMDA receptors are ionotropic...fine...we'll call it non-ionotropic signaling.
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But there's no calcium influx! So what is going on? Some FRET experiments showed that the intracellular tails of the NMDA receptor move in response to glutamate binding, even in the absence of a co-agonist. This certainly smells like metabotropic signaling.
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Recently-ish (Nabavi et al., 2013) it was found that if glutamate binds WITHOUT a co-agonist....LTD can still occur.
(PS - yes, recently-ish was 6-7 years ago...)Prikaži ovu nitHvala. Twitter će to iskoristiti za poboljšanje vaše vremenske crte. PoništiPoništi -
For this next part you need to know something about NMDA receptors: they require TWO agonists for the ion pore to open: (1) glutamate and (2) glycine or D-serine. If glutamate binds the receptor in the absence of the co-agonist the pore does not open and no Ca2+ can flow through.
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Glutamate binds the NMDA receptor, Ca2+ fluxes into the cell and binds PP2B, which dephosphorylates AMPA receptors, leading to AMPA receptor endocytosis and synaptic weakening.
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What is meant by non-ionotropic LTD? Good question. You probably learned that for LTD (and the associated spine shrinkage) to occur, calcium influx through the NMDA receptor is important. This is true.
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Preprint featuring one of the projects I worked on during my time as a research assistant! Here we start to put together the molecular signaling pathway downstream of non-ionotropic LTD and spine shrinkage.https://twitter.com/biorxivpreprint/status/1215319872852414465 …
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