Abstracts

Rationale: Coherent neural oscillations > 30 Hz are present in normal functions, such as gamma binding, as well as network pathology such as epilepsy. Similarly, High Frequency Oscillations (HFOs) > 60 Hz have been identified in both normal and epileptic tissue. However, the mechanisms by which these phenomena form and the distinctions between normal and abnormal HFOs are unknown.Methods: This work uses a physiological computational model to demonstrate that high levels of random synaptic activity can generate HFOs in a locally-coupled network, as well as help spread them to neighboring tissue. Measuring network recruitment required the development of a novel statistical method, which quantified the recruitment generated via preexisting physiological connections such as interneurons, gap junctions, and recurrent axons. Results: Epileptic HFOs, produced by active pyramidal cells with high levels of gap junctions or recurrent axons, recruited neighboring cells provided those cells were exposed to elevated levels of random synaptic activity. Normal HFOs, produced by coherent inhibitory oscillations and sparse pyramidal cell firing, suppressed surrounding tissue and were unable to induce anodal break firing. Conclusions: These findings suggest that synaptic noise and physiological coupling are important for generating and propagating HFOs, and point to a key potential difference between the mechanisms and behavior of normal and epileptic HFOs.