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    This chapter has been cited by the following publications. This list is generated based on data provided by CrossRef.

    Velluti, Julio C Costa da Costa, Jaderson and Russo, Raúl E 1997. The cerebral hemisphere of the turtle in vitro. An experimental model with spontaneous interictal-like spikes for the study of epilepsy. Epilepsy Research, Vol. 28, Issue. 1, p. 29.

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    Yang, Lie and Benardo, Larry S 1998. Removal of superficial inhibition releases hyperexcitability in middle and deep horizontal slices from rat somatosensory neocortex. Neuroscience Letters, Vol. 257, Issue. 1, p. 33.

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    vanDrongelen, W. Lee, H.C. Hereld, M. Chen, Z. Elsen, F.P. and Stevens, R.L. 2005. Emergent Epileptiform Activity in Neural Networks With Weak Excitatory Synapses. IEEE Transactions on Neural Systems and Rehabilitation Engineering, Vol. 13, Issue. 2, p. 236.

    Yang, Lie Benardo, Larry S. Valsamis, Helen and Ling, Douglas S. F. 2007. Acute Injury to Superficial Cortex Leads to a Decrease in Synaptic Inhibition and Increase in Excitation in Neocortical Layer V Pyramidal Cells. Journal of Neurophysiology, Vol. 97, Issue. 1, p. 178.

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    Meijer, Hil GE and Coombes, Stephen 2014. Travelling waves in models of neural tissue: from localised structures to periodic waves. EPJ Nonlinear Biomedical Physics, Vol. 2, Issue. 1,

  • Print publication year: 1993
  • Online publication date: May 2010

12 - Generation of epileptiform discharge by local circuits of neocortex

from Section 3 - ‘Normal’ brain mechanisms that support epileptiform activities



So many books have been written on epilepsy that it may seem rash to add another …

(Jackson, 1874)1

The neuronal essence of seizures is exceptionally synchronous activity. Cortical neurons performing normal tasks tend to fire with relatively low synchrony (Abeles, 1982), but during a seizure the activity of affected neurons is abruptly usurped. The kernel of this idea was suggested by John Hughlings Jackson in the nineteenth century; however, the pathological changes that allow hypersynchrony, and the mechanisms that mediate it, are still elusive (Dichter & Ayala, 1987). Synchrony necessarily requires interactions between neurons, and the most obvious substrate for interaction is synaptic circuitry. Here, we focus on the neurons and circuitry involved in epileptiform activity within the neocortex. The justification for another discourse on the subject is recent research that suggests specific circuit-oriented mechanisms for epileptogenesis.

We begin with a brief description of our experimental model, essentially just an isolated fragment of neocortex in a controlled environment. Our concern is the minimum amount of tissue necessary for epileptiform activity, and in the cerebral cortex that turns out to be a surprisingly small volume.

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