Thus, regulation of Shal/Kv4 channel properties by other proteins, or Shal/Kv4 channel number by activity-dependent trafficking, is likely to translate into changes in neuronal firing output.
Our results suggest that even strong differences in the magnitude of these conductances will not cause qualitatively different firing output in the neurons.
Previous human somatotopy studies using fMRI have been limited not only by scanning resolution [2], [4] but by an underlying premise that fMRI reveals discrete activation "hotspots" in response to cutaneous stimulation [3], [5], like those measured electrophysiologically as the firing output of cells.
Thus, in addition to a role in the firing output of cells, Shal/Kv4 channels, which are localized exclusively to somato-dendritic compartments of cells [23], [24], may function in the dendrites of motoneurons and sensory neurons, modulating the integration of post-synaptic potentials.
However, lower-intensity whisker stimulation revealed a more than 10-fold increase in mean firing output compared with control animals.
Do neurons in adjacent, deprived barrel columns also display a shift in their firing output to different stimulation intensities of the spared whisker?
This is in contrast to neurons in the trigeminal ganglion, which can increase their firing output with increasing stimulus intensity across a broader range (Shoykhet et al., 2000).
Here we investigated how different stimulus intensities modified the firing output of individual neurons in layer 2/3 of the mouse barrel cortex.
Exposure times were measured directly from the Fire output of the EM-CCD using an oscilloscope (TDS 210; Tektronix, Inc., Beaverton, OR).
We assume that HAN firing output is triggered by membrane currents evoked by coreleased OHN transmitters (which generate firing patterns after a further series of interactions with biophysical and geometric properties of the HAN membrane; Haas and Reiner, 1988).
