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Electronic Letters to:
- Neurobiology of Disease:
Pierre-Olivier Polack, Isabelle Guillemain, Emilie Hu, Colin Deransart, Antoine Depaulis, and Stéphane Charpier- Deep Layer Somatosensory Cortical Neurons Initiate Spike-and-Wave Discharges in a Genetic Model of Absence Seizures
J. Neurosci. 2007; 27: 6590-6599[Abstract] [Full text] [PDF]
eLetters: Submit a response to this article
Electronic letters published:
Are absence-related epileptic discharges initiated by layer V or layer VI neurons?
- Didier Pinault (15 July 2007)
Are absence-related epileptic discharges initiated by layer V or layer VI neurons? 15 July 2007 
Didier Pinault,
CR1/Associate Professor
INSERM U666, Fac Med, Strasbourg, 67085, FranceSend letter to journal:
Re: Are absence-related epileptic discharges initiated by layer V or layer VI neurons?
pinault{at}neurochem.u-strasbg.fr Didier Pinault
I read with interest the paper by Polack et al. (J Neuroscience, June 13, 2007). I was surprised to see that the authors did not distinguish in their recordings between layer V and layer VI cells in the “deep layers” of the primary somatosensory (S1) cortex in Genetic Absence Epilepsy Rats from Strasbourg (GAERS). The corticothalamic (CT) cells in these two layers differ greatly morphologically, functionally and in their connectivity. In addition, the authors described a rhythm that gave rise to epileptic discharges, an important finding that was first discovered by my group (Pinault et al., 2001; Pinault, 2003; Pinault et al., 2006). These data, which seems to have been overlooked in the Polack et al.’s paper, are summarized below.
1) Are epileptic discharges initiated by layer V or layer VI neurons in the S1 cortex of GAERS? This question was first addressed in 2003 by Pinault, who demonstrated that morphologically-identified layer VI CT neurons of S1 cortex play an initial role in the generation of epileptic discharges in GAERS. Furthermore, it was shown that layer V cells start to fire in a rhythmic manner after layer VI cells during the generation of epileptic discharges in GAERS. From the Polack et al.’s study (2007) it seems likely that they had actually recorded mainly from layer V cells. The layer V/VI cell shown in Fig2C is clearly a typical pyramidal neuron of layer V.
2) Physiological 9-11 Hz oscillations stated by Polack et al. (2007) “as a prelude of epileptic discharges” in GAERS are very reminiscent of the physiological somatosensory 5-9 Hz oscillations that were originally seen (recorded in freely moving and in anaesthetized rats) to give rise to epileptic discharges in GAERS by Pinault and colleagues (Pinault et al., 2001; Pinault, 2003; Pinault et al., 2006). These previous publications report that the frequency of preictal oscillations, especially in layer VI and in identified layer VI CT neurons, can be up to 12 Hz then suddenly slowing down to 5-9 Hz during their development into epileptic discharges. It is also worth emphasizing that these discharges were also recorded in control non-epileptic rats, and therefore are not specific to GAERS, a point that was also overlooked in the Polack et al.’s paper.
Pinault D, Vergnes M, Marescaux C (2001) Medium-voltage 5-9-Hz oscillations give rise to spike-and-wave discharges in a genetic model of absence epilepsy: in vivo dual extracellular recording of thalamic relay and reticular neurons. Neuroscience 105:181-201.
Pinault D (2003) Cellular interactions in the rat somatosensory thalamocortical system during normal and epileptic 5-9 Hz oscillations. J Physiol 552:881-905.
Pinault D, Slezia A and Acsady L (2006) Corticothalamic 5-9 Hz oscillations are more pro-epileptogenic than sleep spindles in rats. J Physiol Lond 574, 209-227.
Polack PO, Guillemain I, Hu E, Deransart C, Depaulis A, Charpier S (2007) Deep layer somatosensory cortical neurons initiate spike-and-wave discharges in a genetic model of absence seizures. J Neurosci 27:6590- 6599.
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