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The Journal of Neuroscience, March 28, 2007, 27(13):3383-3387; doi:10.1523/JNEUROSCI.0145-07.2007
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Brief Communications
Feedforward Inhibition Contributes to the Control of Epileptiform Propagation Speed
Andrew J. Trevelyan,1,2 David Sussillo,1 andRafael Yuste1 1Department of Biological Sciences, Howard Hughes Medical Institute, Columbia University, New York, New York 10027, and 2School of Neurology, Neurobiology, and Psychiatry, The Medical School, University of Newcastle, Newcastle NE2 4HH, United Kingdom
Correspondence should be addressed to Andrew J. Trevelyan at his present address: School of Neurology, Neurobiology, and Psychiatry, The Medical School, University of Newcastle, Newcastle NE2 4HH, UK. Email: andytrev{at}gmail.com
It is still poorly understood how epileptiform events can recruit cortical circuits. Moreover, the speed of propagation of epileptiform discharges in vivo and in vitro can vary over several orders of magnitude (0.1–100 mm/s), a range difficult to explain by a single mechanism. We previously showed how epileptiform spread in neocortical slices is opposed by a powerful feedforward inhibition ahead of the ictal wave. When this feedforward inhibition is intact, epileptiform spreads very slowly (
100 µm/s). We now investigate whether changes in this inhibitory restraint can also explain much faster propagation velocities. We made use of a very characteristic pattern of evolution of ictal activity in the zero magnesium (0 Mg2+) model of epilepsy. With each successive ictal event, the number of preictal inhibitory barrages dropped, and in parallel with this change, the propagation velocity increased. There was a highly significant correlation (p < 0.001) between the two measures over a 1000-fold range of velocities, indicating that feedforward inhibition was the prime determinant of the speed of epileptiform propagation. We propose that the speed of propagation is set by the extent of the recruitment steps, which in turn is set by how successfully the feedforward inhibitory restraint contains the excitatory drive. Thus, a single mechanism could account for the wide range of propagation velocities of epileptiform events observed in vitro and in vivo.
Key words: epilepsy; seizure; calcium imaging; inhibition; pyramidal cell; neocortex
Received Nov. 3, 2006; revised Feb. 12, 2007; accepted Feb. 13, 2007.
Correspondence should be addressed to Andrew J. Trevelyan at his present address: School of Neurology, Neurobiology, and Psychiatry, The Medical School, University of Newcastle, Newcastle NE2 4HH, UK. Email: andytrev{at}gmail.com
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