(where corticospinal would be) v1 l5 projects to sup colliculus
emx2 pax6
spinal cord: diff genes express in specific subpopulations in progenitors in spinal cord progenitors, but not in cortex
bishop et al science 2000, j of neurosci 2002
lx2 something f1
pmbsf barrels "co histochemistry" p7 serotonin immunohistostaining
rorb
changing emx2 does not cause chimeric nrns
cad8 mega1
note: wang and burkhalter higher order areas get too close to S1, mb A -- suggest multimodality (which that other paper confirms anyway).
visalp, visam, visi are the ones oleary likes out of the genes he has
coup-tf1
note: things like coup-tf1 deletion seem more like tuning than basic property; are there severse deficits in phenotype? also, who do emx2- mice die?
mdga1
emx2 vis+, coup-tf1 motor-
sp8, pax 6 are s1-, motor+??
oleary's model is a total ordering of areal dominance
my alternate hypothesis why making motor areas larger hurts performance: mb 2nd-order areas get hurt