A comparison of recurrent inhibition and of paired-pulse facilitation in hippocampal slices from normal and genetically epileptic mice
Identifieur interne : 001399 ( Main/Exploration ); précédent : 001398; suivant : 001400A comparison of recurrent inhibition and of paired-pulse facilitation in hippocampal slices from normal and genetically epileptic mice
Auteurs : George Kostopoulos [Grèce] ; George Antoniadis [Grèce]Source :
- Epilepsy Research [ 0920-1211 ] ; 1991.
Abstract
Tottering mice exhibit inherited generalized epilepsy of the ‘absence’type. In hippocampal slices from these mutant mice studied in vitro, pairing an alvear antidromic stimulus to an orthodromic one revealed a strong recurrent inhibition (RI) of CA1 pyramidal neurons. RI was maximal at 10 ms inter-pulse interval (IPI 70% decrease of population spike, PS) gradually decreasing to 15% at 320 ms IPI. At 10 ms IPI it shifted the input/output curves to the right and decreased maximum PS. In the group of slices from epileptic mice the early part of RI (2.5–60 ms) was indistinguishable from that of normal mice, with respect to both its strength and its lability to activity-dependent decrement induced by a train of antidromic stimuli (8 s, 5 Hz). However, the delayed part (80–320 ms) was slightly stronger in the epileptic group. Also in this group only the train of antidromic pulses caused a significant and lasting decrease in the unconditioned orthodromic PS. Paired-pulse facilitation was equally strong in the 2 groups of slices. It is concluded that mechanisms underlying epileptogenic hyperexcitability in the tottering mutant may not include a failure of inhibition, at least in the CA1 area of the hippocampus. On the contrary some inhibitory mechanisms may be stronger.
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DOI: 10.1016/0920-1211(91)90052-H
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In hippocampal slices from these mutant mice studied in vitro, pairing an alvear antidromic stimulus to an orthodromic one revealed a strong recurrent inhibition (RI) of CA1 pyramidal neurons. RI was maximal at 10 ms inter-pulse interval (IPI 70% decrease of population spike, PS) gradually decreasing to 15% at 320 ms IPI. At 10 ms IPI it shifted the input/output curves to the right and decreased maximum PS. In the group of slices from epileptic mice the early part of RI (2.5–60 ms) was indistinguishable from that of normal mice, with respect to both its strength and its lability to activity-dependent decrement induced by a train of antidromic stimuli (8 s, 5 Hz). However, the delayed part (80–320 ms) was slightly stronger in the epileptic group. Also in this group only the train of antidromic pulses caused a significant and lasting decrease in the unconditioned orthodromic PS. Paired-pulse facilitation was equally strong in the 2 groups of slices. It is concluded that mechanisms underlying epileptogenic hyperexcitability in the tottering mutant may not include a failure of inhibition, at least in the CA1 area of the hippocampus. On the contrary some inhibitory mechanisms may be stronger.</div></front></TEI><affiliations><list><country><li>Grèce</li></country></list><tree><country name="Grèce"><noRegion><name sortKey="Kostopoulos, George" sort="Kostopoulos, George" uniqKey="Kostopoulos G" first="George" last="Kostopoulos">George Kostopoulos</name></noRegion><name sortKey="Antoniadis, George" sort="Antoniadis, George" uniqKey="Antoniadis G" first="George" last="Antoniadis">George Antoniadis</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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