This work hopefully identifies new models of neurodevelopmental conditions which can revolutionise future research.

With insane support from @sidb-edinburgh.bsky.social @edinunineuro.bsky.social @ukri.org @patrickwildcentre.bsky.social

and help from @vectorbuilder.bsky.social

This work has been championed by Max Knops and @sorayam.bsky.social, and many other colleagues, not limited to: Max Wilson, @bonthronphd.bsky.social @l-w-taylor.bsky.social
Alsadeg Bilal, Imran Liaquat, Paul Brennan, @clairedurrant1.bsky.social

This work was led by Ania Sumera and Laura Oliveira, but with help from immensely talented students and collaborators, and @edinunineuro.bsky.social @sidb-edinburgh.bsky.social

Despite an absence of AIS shortening in response to sustained activity modulation, we do see other functional changes associated with homeostatic plasticity - including changes in membrane excitability and NMDA receptor function

And amazing collaborators @clairedurrant1.bsky.social @sorayam.bsky.social @l-w-taylor.bsky.social among many others not on here :)

This work would not be possible without the patients, our funders @sidb-edinburgh.bsky.social, UK MRC, @edinunineuro.bsky.social

Finally, we show show that GABAB receptor currents are elevated in patients who receive the anti-seizure medication Levetiracetam - regardless of seizure history.

Further, we show that presynaptic GABAB receptors signalling is stronger in human cortical inputs than rodents. This leads to differential control of cortical oscillations.

In this we find that postsynaptoc GABAB receptors signalling undergoes developmental maturation in cortical columns, but is largely stable over adult human life.

True, but if many of the facets of microglial function have been attributed to their role in mouse brain circuits, then perhaps not all is as it seems. A conditional FIRE mouse or rat could/would approach an answer

That is an interesting point. That being said rats lacking the CSF1R gene survive pretty well... see Patkar et al 2021 ... But with some deficits in neuronal progenitors. More to do!