As a whole, our in utero injection experiments confirm that NeuroD1 has a stronger neuron-inducing effect than Ngn2 when overexpressed in hippocampal progenitors.
These reporters exhibited more restricted expression patterns, with strong sensory neuron expression (Fig. 5A, wt panels).
If this mechanism would be solely responsible for ALS pathogenesis, gene knockdown or knockout is expected to result in strong motor neuron phenotypes.
Consistent with these experiments, in our hands, overexpression of TBPH with a strong motor neuron driver induced locomotion defects and also resulted in TBPH being predominantly expressed in the cytoplasm.
Unlike DOR-eGFP that predominantly localizes at the plasma membrane under basal conditions (Scherrer et al. 2006; Pradhan et al. 2009), the MOR-mcherry fluorescent signal was strong inside neurons (Fig. 2a) and rather weak at the plasma membrane.
This pattern was complementary to that of thalamic input from VL, that is, callosal input was strong to neurons in L2/3 and weak to those in L4, and vice versa for VL input.
First, the effects are strongest for neurons and neuronal domains responsive to cardinal stimuli, in particular the vertically oriented stimuli; and second, when stimulating the hemifield contralateral to the recording (the noncooled hemifield), the cooling effects are negligible.
There is strong evidence that neuron identity, neuron type and laminar fate are already specified, before the onset of migration towards the pial surface [ 23, 24].
The ventral ganglion contains 3 pairs of strong PRXa-IR neurons (Va neurons): a bilateral pair of these Va neurons is located ventrally in each of the first three abdominal neuromeres.
We note, however, that the pattern of the noise correlations is not entirely unstructured because the correlations are slightly but significantly stronger between neurons with RFs on the same curve than between neurons with RFs on different curves (see also Roelfsema et al. 2004).
