Temporal lobe epilepsy (TLE) is often accompanied by interictal behavioral abnormalities, such as fear and memory impairment. To identify possible underlying substrates, we analyzed long-term synaptic plasticity in two relevant brain regions, the lateral amygdala (LA) and the CA1 region of the hippocampus, in the kindling model of epilepsy. Wistar rats were kindled through daily administration of brief electrical stimulations to the left basolateral nucleus of the amygdala. Field potential recordings were performed in slices obtained from kindled rats 48 h after the last induced seizure, and in slices from sham-implanted and nonimplanted controls. Kindling resulted in a significant impairment of long-term potentiation (LTP) in both the LA and the CA1, the magnitude of which was dependent on the number of prior stage V seizures. Saturation of CA1-LTP, assessed through repeated spaced delivery of high-frequency stimulation, occurred at lower levels in kindled compared to sham-implanted animals, consistent with the hypothesis of reduced capacity of further synaptic strengthening. Furthermore, theta pulse stimulation elicited long-term depression in the amygdala in nonimplanted and sham-implanted controls, whereas the same stimulation protocol stimulation caused LTP in kindled rats. In conclusion, kindling differentially affects the magnitude, saturation, and polarity of LTP in the CA1 and LA, respectively, most likely indicating an activity-dependent mechanism in the context of synaptic metaplasticity.Convulsive diseases in humans such as temporal lobe epilepsy (TLE) are often accompanied by impairments of learning and memory. In addition, TLE patients typically display emotional disturbances, in particular negative emotions such as fear, anxiety, and depression (Kalynchuk 2000). A wealth of data has established that the amygdala plays a critical role in neuronal activity and synaptic plasticity related to both emotionally modulated signal processing and epilepsy (Gloor 1990;Maren 1999;LeDoux 2000). Synapses in the amygdala display long-term potentiation (LTP) (Chapman and Chattarji 2000; LeDoux 2000; Maren 2001), a long-lasting increase of synaptic strength that is widely believed to be a cellular basis of learning and memory (Bliss and Collingridge 1993). The amygdala possesses the lowest threshold for the induction of kindling (Löscher 1997), an established experimental model of TLE in which daily electrical stimulation results in a gradual progression and intensification of limbic motor seizures (Goddard et al. 1969). Although kindling has been extensively investigated in the context of its clinical relevance to epilepsy and seizure-induced synaptic potentiation, only a few studies that relate to plastic synaptic changes after kindling are available. Therefore, the present study was undertaken to systematically analyze the influence of kindling 48 h after the last seizure on long-term synaptic plasticity, LTP, and long-term depression (LTD) in the lateral nucleus of the amygdala (LA) in rats. The LA was chosen ...
