Our results raise two related issues. First, the delivery of the GluA1 subunit to the surface of CA1 pyramidal neurons requires CNIHs. Yet this is clearly not the case in heterologous expression systems. What accounts for the difference? The situation may be analogous to TARP γ-2, which is essential for the surface delivery of AMPARs in cerebellar granule neurons and greatly facilitates surface delivery of AMPARs in heterologous cells, but is not essential for their delivery. Second, can the results obtained in CA1 pyramidal neurons be applied to other neurons? Our results suggest that CNIH-2 plays a similar role in AMPAR trafficking in both dentate granule neurons and layer 2/3 neocortical neurons. However, these neurons are likely to be similar to CA1 neurons in their expression of GluA1A2 heteromers and TARP γ-8. Is there an example of a neuron that expresses GluA1 subunits but not CNIH-2? Our results would suggest not, since the surface expression of GluA1 in neurons requires CNIH-2. Also of interest are Purkinje neurons, which express high levels of CNIH-2, but only transiently express GluA1 (Douyard et
