Overall, our slice recordings from the SMA model mice suggest that by P5 P6 many motor neurons in the ventral spinal cord are no longer active, and those that remain are less active overall and less able to be stimulated by modulating agents.
Our data indicate that α2 Na,K-ATPase remains in the membrane and is able to be stimulated by other regulatory pathways including its interaction with the nAChR.
The clonal cells containing the IE 3T LAI LTR and 5T LAI LTR were able to be stimulated with TNF- α to drive higher levels of GFP expression.
The authors described the morphology of these nerve cells in detail, but the functional proof, namely, in how far these cells exhibited spontaneous action potential and/or were able to be stimulated, is still lacking.
Both IE and HE cell clones containing the WT, 3T, or 5T LTRs were able to be stimulated resulting in an increase in LTR-driven GFP expression compared to basal activity).
As a confirmation that α2 Na,K-ATPase remains in the membrane and is functional after HS, we tested whether the Na,K-ATPase α2 isozyme is able to be stimulated by nanomolar concentrations of nicotinic acetylcholine receptor (nAChR) agonists, an effect shown previously [ 24, 25].
