Biophysical Aspects of the Nonsynaptic Epileptiform Activity

Since the demonstration that the hippocampus slice exposed to low calcium external solution is able to sustain nonsynaptic epileptiform activity, it has been accepted that nonsynaptic interactions may be sufficient, in some conditions, for generating seizure like activity in cortical network. Recently, evidences have suggested that the reductions in calcium are not essential for nonsynaptic mechanisms to contribute to epileptic activity. Therefore, evidences allow demonstrating that the conjoint actuation of nonsynaptic mechanisms and nonsynaptic connections are able to induce and sustain seizures. The nonsynaptic mechanisms considered in this context are all mechanisms which are not directly involved with synaptic transmission, but comprehending important action on the homeostasis equilibrium and, consequently, on the neuronal excitability. The non-synaptic connections are all types of neuronal coupling that are not mediated by synaptic transmission. The concomitant actuation of nonsynaptic mechanisms and connections seems to be a relevant process for the seizure intensity modulation. Therefore, it may be conjectured that the nonsynaptic mechanisms and connections could be considered a natural target for investigations aiming to control refractory seizures. Within this perspective, the scope of the present chapter will cover the following topics: • nonsynaptic events: experimental induction and electrophysiological characteristics; • nonsynaptic mechanisms; • nonsynaptic connections; • biophysical aspects of the nonsynaptic epileptiform activities; • possible targets for controlling refractory seizures.