This chapter is about the intrinsic neuronal properties and network operations that underlie different forms of seizures. The antagonism between concepts emphasizing the “epileptic neuron” or “epileptic networks” is obsolete as both voltage-gated properties of single neurons and synaptic articulations within different forebrain structures (neocortex, thalamus, corticothalamic loops, archicortex, and related systems) are crucial for the generation and spread of electrical paroxysms.

The knowledge of intrinsic cell properties has continuously evolved due to in vitro work conducted in the neocortex, thalamus, and hippocampus. A series of studies pointed to various ionic currents that are implicated in potentiating the susceptibility to seizures.

The discovery of voltage-dependent Na+ and Ca2+ channels in dendrites changed the model of dendrites with only passive properties and demonstrated that different intrinsic currents can amplify synaptic signals, which may eventually lead to abnormal cellular excitation and paroxysmal discharges.

The intrinsic propensity of some neocortical and hippocampal neurons to bursting is also a factor that predisposes to seizures. In fact, there is a continuum of variation in burstiness of cortical neurons. In vivo experiments, using intracellular recordings in acutely prepared and chronically implanted animals, have shown different incidences of intrinsically bursting (IB) neurons in different experimental conditions, depending on the degree of background firing, as well as the transformation of IB into regular-spiking (RS) neurons with enhanced synaptic activity (see 2.1.2 and 2.1.3 in Chapter 2). In vitro, the continuum extends from non-bursters to bursters that are induced by extrinsic depolarization as well as to spontaneously bursting neurons.