Epilepsy is a chronic disorder characterized by spontaneously recurrent seizures. Its most prevalent form, temporal lobe epilepsy (TLE), often originates in the hippocampus and/or amygdala and is frequently associated with profound fear and anxiety disorders. Also, a panic attack and an epileptic seizure can share many of the same symptoms. Recently, it has been shown that fear conditioned learning potentiates synaptic transmission in the lateral amygdala of rodents. Furthermore, we have found that hippocampal epileptic activity can also cause potentiation of synaptic transmission between CA3 pyramidal cells. From these findings we hypothesize that TLE causes fear and anxiety disorders through long-lasting changes in synaptic transmission in the lateral amygdala (LA). To test our hypothesis, we used a horizontal slice preparation of the rodent brain which includes the hippocampus and amygdala as well as preserved interconnections. Within this preparation we studied the spreading of epileptic bursts by means of c-fos expression as well as multiple extracellular and whole-cell patch-clamp recordings. We found spreading of epileptic activity between hippocampus, perirhinal cortex and lateral and basolateral amygdala with varying delay times in between burst-onsets. This suggests the existence of a number of different networks underlying the spreading of bursts. We also looked at the long term effects of this epileptic activity on cellular excitability and synaptic transmission in the LA, and found significant differences in the amplitudes of excitatory postsynaptic currents. Interestingly, the nature of these changes depended on the cell type from which the measurements were made. Thus, pyramidal cells with so-called 'highly adapting' spiking patterns underwent a decrease in amplitude, while pyramidal cells with 'little adapting' spiking patterns showed increases in amplitudes. These different spiking patterns, thought to be caused by the absence or presence of a slow after hyperpolarizing current, thus seem to have a differential effect on the induction of changes in synaptic strength.