PENTYLENETETRAZOL KINDLING CHANGES THE ABILITY TO INDUCE POTENTIATIONPHENOMENA IN THE HIPPOCAMPAL CA1 REGION

Citation
M. Krug et al., PENTYLENETETRAZOL KINDLING CHANGES THE ABILITY TO INDUCE POTENTIATIONPHENOMENA IN THE HIPPOCAMPAL CA1 REGION, Physiology & behavior, 62(4), 1997, pp. 721-727
Citations number
47
Categorie Soggetti
Psychology, Biological","Behavioral Sciences",Physiology
Journal title
ISSN journal
00319384
Volume
62
Issue
4
Year of publication
1997
Pages
721 - 727
Database
ISI
SICI code
0031-9384(1997)62:4<721:PKCTAT>2.0.ZU;2-V
Abstract
The present study describes changes of response enhancement of hippoca mpal field potentials in slices of kindled rats using different method s to induce long-lasting potentiation. Eight-week-old male Wistar rats were subjected to pentylenetetrazol (PTZ) kindling induced by intrape ritoneal injection of 45 mg/kg once every 48 h until the occurrence of seizure stages 4-5. Eight to twelve days after the last kindling sess ion, transverse hippocampus slices were prepared and maintained in an artificial medium. Evoked-field potentials were recorded in the CA1 re gion upon stimulation of the Schaffer collaterals. Potentiation was in duced: 1. By moderate tetanic stimulation of the Schaffer collaterals, 2. by changing the perfusion medium to 0-magnesium for 30 min, and 3. by changing the medium to 4 mM Ca2+ for 7 min. In slices from kindled rats, long-term potentiation (LTP) after tetanic stimulation and incr ease of the evoked potential by 0-magnesium were significantly enhance d in comparison to slices from sham-kindled rats. However, Ca2+-induce d LTP could not be induced in slices from kindled rats. The results su pport the assumption that PTZ kindling also induces lasting changes in the responsiveness of hippocampal structures, expressed as an enhance d ability to induce potentiation. An alteration of N-methyl-D-aspartat e (NMDA) receptor-coupled processes can be assumed. The inability to i nduce Ca2+-induced LTP points to more complex effects of PTZ, perhaps also on nonNMDA coupled ionic channels. (C) 1997 Elsevier Science Inc.