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Generators of Focal Epileptic Activity in the Buccal Ganglia of Helix Pomatia

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For more content, see Archives Néerlandaises de Zoologie (Vol 1-17) and Animal Biology (Vol 53 and onwards).

Induction and spread of epileptic activity was studied in the buccal ganglia of Helix pomatia used as model nervous system. Epileptic activity was induced by application of epileptogenic drugs. With increasing epileptogenicity, i.e. increasing concentration of an epileptogenic drug, typical epileptic depolarizations (PDS) appeared first in the identified neuron B3 and subsequently in neurons B1 and B2. At high concentrations of the drugs large numbers of neurons generated epileptic activity. PDS were found to be primarily synchronized within the networks of electrically coupled neurons. Comparing the activities in the different networks, they were independent from one another and thus corresponded to multi-focal seizure activities in man. In the identified neuron B4 no PDS were recorded. Processes are described which are anti-epileptic and epileptogenic in effect. Thus, with enduring application of the drugs, epileptic activity decreased slowly during several hours. With repeated applications of the drugs, i.e. when there were intervals of wash-out of the drugs, epileptic activity could be increased. Comparing the activity of epileptic neurons with that of non-epileptic ones, non-epileptic neurons became progressively coupled to the epileptic rhythms. This coupling increased during up to one day. It could indicate first steps in the establishment of a generator of epileptic activity in nervous systems.

Affiliations: 1: Institut fur Experimentelle Epilepsieforschung, Universitit Münster, Hüfferstr. 68, 48149 Müns-ter, Germany; 2: Institut für Physiologie, Universität Münster, Robert-Koch-Str. 27a, 48149 Müns-ter, Germany; 3: Institut fur Experimentelle Epilepsieforschung, Universitit Münster, Hüfferstr. 68, 48149 Müns-ter, Germany, Institut für Physiologie, Universität Münster, Robert-Koch-Str. 27a, 48149 Müns-ter, Germany

10.1163/156854293X00467
/content/journals/10.1163/156854293x00467
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/content/journals/10.1163/156854293x00467
1993-01-01
2016-12-05

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