Abstract

In many studies a fundamental difference between two types of generalized epileptic activity, convulsive epilepsy and absence non-convulsive epilepsy was described. All forms of convulsive epilepsy, both in human and animal models, are characterized by increased activity of excitatory amino acid transmitter systems (Hara et al., 2006; Leke et al., 2006; Schilling et al., 2006) and/or decreased activity of the inhibitory GABAergic system (Bazyan et al., 2001b; Quilichini et al., 2006; Laschet et al., 2007) of the brain. The main difference between absence non convulsive epilepsy and convulsive epilepsy is in a fact that pharmacological stimulation or inhibition of excitatory glutamate synaptic transmission causes relative enhancement or reduction of the severity of absence epilepsy (Ngomba et al., 2005; Citraro et al., 2006), and increased GABAergic inhibition also leads to enhanced absence epilepsy (Coenen et al., 1995; Bouwman et al., 2003; 2004). The next fundamental difference between absence epilepsy and other generalized epilepsy forms consists in the profile of epileptic discharge. Usually, convulsive epileptic discharges appear on the wave of excitation. The gradual growth of excitation reaches the threshold level after which epileptic discharges appear. During absence epilepsy, the discharge is fundamentally different. A spike–wave discharge consists of an inhibitory phase and an action potential. The inhibitory phase is represented by a slow wave on an EEG. The spike is an indicator of cell excitation (action potential). A rebound spike appears at the end of the inhibitory period, and the cycle repeats again and again (Midzianovskaya et al., 2001). In this paper we compared mechanisms underlying two kinds of epileptic activity, pentylenetetrazole kindling and absence epilepsy, and their interaction with processes of learning, memory, emotional and motivational states.

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