On Monday, March 3rd, Erin Munro from the RIKEN Brain Science Institute
in Wakoshi, Japan will be visting. She will be giving two talks- one at
noon and one at
Title: Subthreshold somatic voltage in neocortical pyramidal cells can control whether spikes propagate from the axonal plexus to axon terminals: a model study.
Abstract: There is suggestive evidence that pyramidal cell axons in neocortex may be coupled by gap junctions into an “axonal plexus” capable of generating very fast oscillations (VFOs) with frequencies exceeding 80 Hz. It is not obvious, however, how a pyramidal cell in such a network could control its output when spikes are free to propagate from the axons of other pyramidal cells into its own axon. We address this problem by means of simulations based on three-dimensional reconstructions of pyramidal cells from rat somatosensory cortex. We show that high somatic voltage enables propagation via gap junctions into the initial segment and main axon, while low somatic voltage disables it. We show further that somatic voltage cannot effectively control spike propagation through gap junctions on minor collaterals; spikes may therefore propagate freely from such collaterals regardless of somatic voltage. In previous work, VFOs are all but abolished during the down phase of slow oscillations induced by anesthesia in vivo. This finding constrains the density of gap junctions on collaterals in our model. Furthermore, it suggests that axonal sprouting due to cortical lesions may result in abnormally high gap junction density on collaterals, leading in turn to excessive VFO activity and hence to epilepsy via kindling.
4 pm talk
Title: Independent neural sources reveal two different slow oscillations.
Abstract: Sleep has multiple stages including slow-wave sleep and REM sleep. Slow-wave sleep is characterized by a large amplitude slow oscillation (<2 Hz) seen throughout the cortex. Within the slow oscillation UP phases are characterized by global spiking while DOWN phases are characterized by global silence. Currently there is a debate as to whether this slow oscillation is generated by the cortex alone or through interactions between the thalamus and cortex. In our study, rats were anesthetized with urethane anesthesia, which induced a slow oscillation similar to slow-wave sleep. Recordings were taken with a 32 channel silicon probe inserted vertically into the auditory cortex. To analyze neocortical state, we applied independent component analysis (ICA) to the current source density (CSD) derived from the recordings. ICA separates the CSD into temporally independent neural sources and gives a spatial profile of how the time series of each source is projected onto the recording electrodes. In this manner, many overlapping sources in the original CSD are revealed and can be studied individually. ICA consistently identified 2 sources across experiments: a strong broad source centered in layer 5 (BL5), an apparent sub-cortical source producing a clock-like 3.5 Hz oscillation (SUB). By focusing on the BL5 and SUB sources, we are able to distinguish two different slow oscillations. One slow oscillation is dominated by the BL5 source, UP phases are initiated by a source in the deeper layers similar to propagating waves seen during cortically generated spontaneous activity. The SUB source does not oscillate. The other slow oscillation is characterized by a clock-like oscillation in the SUB source, and UP phases in the CSD are generated by another broad source while the BL5 source is not active. These findings suggest that two distinct mechanisms for the slow oscillation are at work in the cortex - at different times of sleep.
- The OWU Programming Contest will be held Saturday, March 22nd, 2014. More information can be found here