Abstract
Computational models of gamma oscillations have helped increase our understanding of the mechanisms that shape these 40–80 Hz cortical rhythms. Evidence suggests that interneurons known as basket cells are responsible for the generation of gamma oscillations. However, current models of gamma oscillations lack the dynamic short term synaptic plasticity seen at basket cell-basket cell synapses as well as the large autaptic synapses basket cells are known to express. Hence, I sought to extend the Wang-Buzsáki model of gamma oscillations to include these features. I found that autapses increased the synchrony of basket cell membrane potentials across the network during neocortical gamma oscillations as well as allowed the network to oscillate over a broader range of depolarizing drive. I also found that including realistic synaptic depression filtered the output of the network. Depression restricted the network to oscillate in the 60–80 Hz range rather than the 40–120 Hz range seen in the standard model. This work shows the importance of including accurate synapses in any future model of gamma oscillations.
Highlights
Gamma oscillations are signals at 40–80 Hz that can be recorded in the hippocampus and neocortex [1]
All previous models of gamma oscillations have ignored the presence of autaptic connections, and I sought to test whether autapses help to enhance the synchrony of interneuron activity during gamma oscillations
Our network simulation indicates that autapses enhance the synchrony of basket cell networks when they oscillate in the gamma range (40–80 Hz)
Summary
Gamma oscillations are signals at 40–80 Hz that can be recorded in the hippocampus and neocortex [1]. As reviewed by Tiesinga and Sejnowski [11], the pyramidal-interneuron gamma (PING) model specifies that the excitatory drive has a larger effect on pyramidal neurons, which in turn activate local basket cells. These inhibitory cells feed back to pyramidal cells, inhibiting them for one gamma cycle. The PING model differs from the WB model, in that excitatory traffic into the system targets pyramidal cells, rather than targeting interneurons It is currently unclear which of these models likely represents the true mechanism in the neocortex, and potentially both are viable, depending on the physiological state of the cortex [11]. I sought to investigate the consequence of including autaptic connections and realistic synaptic depression in a neocortical model of gamma oscillations
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