A Neural Precedent

Seizures are extremely debilitating for patients of conditions such as epilepsy, and though some episodes can be attributed to external triggers, such as stress, physical exertion or certain medications, others appear to have no outside influence. Whatever the trigger, the rapid shift from healthy to ictal activity is not fully understood, and so remains a keen area of research interest. Conventional wisdom suggests that the loss of GABA receptor inhibition in normal physiological function is the key to understanding the process; but new research from a group at Yale suggests that there may be more to the story than previously thought (1).

The authors demonstrated that changes occur within three distinct subpopulations of hippocampal GABAergic interneurons (SST, PV and RT) prior to ictal onset. Moreover, differences in pre-ictal firing patterns within these subtypes in the hippocampal circuit may demonstrate a more finely tuned system of inhibition that drives ictal behavior, when lost. “These findings highlight the complex involvement of distinct GABAergic interneuron populations in the early stages of pathological activity in the hippocampus,” state the researchers in the paper. The hope, they say, is that this early work will drive investigations of other inhibitory cell types, which have yet to be Investigated. Ictal onset may be more complex than previously assumed. Specific cell subpopulation activity may underpin a finer level of tuning, which will require further investigation before it can be translated into the clinic.