Abstract
The relationship between kindling and chronic epilepsy with spontaneous seizures remains uncertain. Kindling is never observed as a natural phenomenon, but can easily be induced in any vertebrate species by stimulation of discrete brain sites. Focal brain lesions such as trauma or ischemia frequently lead to epilepsy after a delay of several weeks to months. Several models of status epilepticus (SE) which induce hippocampal and extrahippocampal lesions can also lead to chronic epilepsy after a delay of four weeks to four months (McIntyre et al., 1982; Leite et al., 1990; Vicedomini and Nadler, 1987; 1990; Lothman and Bertram, 1993; Shirasaka and Wasterlain, 1994; Milgram et al., 1995). This delay in the development of post traumatic and post lesional epilepsy has given rise to the speculation that lesions damage an antikindling filter, so that after some types of focal brain damage, kindling or over kindling (Milgram et al., 1995) takes place spontaneously, perhaps as a result of loss of inhibition around the lesion, and leads to chronic epilepsy. If this is true, epileptogenic lesions should lead to a facilitation of kindling and to an enhancement of long term potentiation (LTP) during the latent period between the occurrence of damage and that of spontaneous epileptic seizures. In the current study, we used the perforant path stimulation model of status epilepticus (Sloviter, 1991; Shirasaka and Wasterlain, 1994) and show facilitation of both kindling and perforant path LTP during the latent period following an epileptogenic hippocampal lesion induced by perforant path stimulation.
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Wasterlain, C.G., Mazarati, A.M., Shirasaka, Y., Sankar, R., Thompson, K.W. (1998). Facilitation of Kindling and Long Term Potentiation by Hippocampal Lesions. In: Corcoran, M.E., Moshé, S.L. (eds) Kindling 5. Advances in Behavioral Biology, vol 48. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5375-5_36
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DOI: https://doi.org/10.1007/978-1-4615-5375-5_36
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