Happy #FluorescenceFriday from this pair of white-matter oligodendrocytes!

New cell-type for #FluorescenceFriday: astrocytes in the cerebral cortex

Which track do I choose: On #FluorescenceFriday, a pair of newly formed oligodendrocytes encounter a field of neuronal axons. Later in development, they will wrap around and insulate subset of these axons

Celebratory #FluorescenceFriday this week, with the JNeurosci cover featuring an image from our article on how Mef2c controls intracortical projection targeting

Bittersweet #FluorescenceFriday saying goodbye to the Kolodkin lab with one last image, this time from the retinal side side of the lab. Here's a collection of retinorecipient targets in the mouse brain. How many of them can you name?

'From thought to action'... axons from the sensory cortex (green) arrive in the motor region to synapse with target neurons (yellow). Can't wait to get back to more imaging after weeks of thesis writing #FluorescenceFriday

Also, reducing the levels of repulsive ligand EfnA5 in the opposite (target) hemisphere restored targeting by Mef2c mutant neurons (10/n)

Overexpressing EphA6 in otherwise normal callosal neurons also reduces their contralateral targeting; disrupting EphA6 signaling partly restores targeting by Mef2c mutant neurons (9/n)

We reasoned that Mef2c mutants fail to project to the opposite somatosensory cortex because of this misregulation of EphA receptor expression (8/n).

Looking at transcriptional profiling from Christopher Cowan’s lab, we were struck by the upregulation of EphA repulsive guidance receptors upon Mef2c loss. The somatosensory cortex has high levels of repulsive ligand EphrinA5, compared to more medial regions. (7/n)

Curiously, initial axon growth into the corpus callosum and midline crossing are unaffected. The target innervation step is specifically compromised. (6/n)

Instead, their projections are shifted to the more medial cingulate cortex. Projection to other targets is also disrupted.(4/n)

Deleting Mef2c specifically in callosal neurons of the somatosensory area in one cortical hemisphere compromises their ability to connect to the somatosensory cortex on the opposite side.(4/n)

Mef2c is highly expressed in callosal neurons, which connect the two hemispheres of the cerebral cortex, just as they’re starting to elaborate their axonal projections.(3/n)

Happy to share our pre-print, “ Mef2c controls postnatal callosal axon targeting by regulating sensitivity to Ephrin Repulsion”. We found that the topography of interhemispheric connectivity in the cerebral cortex is disrupted upon Mef2c deletion.(1/n)