Introduction

Electrophysiological techniques together with pharmacological procedures have been used extensively to explore the basic mechanisms that underlie the generation of synchronous neuronal activity characteristic of epilepsy (for reviews, see Jasper et al., 1969; Schwartzkroin & Wheal, 1984; Delgado-Escueta et al., 1986; Avoli et al., 1990). In the course of these studies different procedures have been employed to elicit epileptiform activity and, as a result, several models have been developed. These include experimental paradigms in which the processes associated with acute or chronic epileptogenesis can be analyzed by using in-vivo as well as in-vitro preparations. In addition, electrophysiological studies have been performed in genetic models where seizure activity is related to the predisposition of a given animal strain to epileptic attacks, either spontaneously or following physiological stimuli (Kostopoulos & Psarropoulou, 1990; see also Chapter 3, this volume).

The relevance of any mechanism discovered in these studies for understanding the physiopathogenesis of human epileptic syndromes depends on the demonstration that such mechanisms also characterize the human condition. For instance, while it is undisputed that the impairment of γ-aminobutyric acid (GABA) synthesis leads to seizures (Molony & Paramelee, 1954), a decreased efficacy of GABAergic potentials in focal, chronic epilepsy is still a matter of debate (cf. Avoli, 1988; see also p. 266, below).