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Long‐lasting modification of intrinsic discharge properties in subicular neurons following status epilepticus
Author(s) -
Wellmer Jörg,
Su Hailing,
Beck Heinz,
Yaari Yoel
Publication year - 2002
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2002.02086.x
Subject(s) - subiculum , bursting , neuroscience , status epilepticus , depolarization , hippocampus , chemistry , seizure threshold , afterdepolarization , pilocarpine , electrophysiology , epilepsy , psychology , biophysics , biology , anticonvulsant , dentate gyrus , repolarization
A single episode of status epilepticus (SE) induces neuropathological changes in the brain that may lead to the development of a permanent epileptic condition. Most studies of this plasticity have focused on the hippocampus, where both synaptic function and intrinsic neuronal excitability have been shown to be persistently modified by SE. However, many other brain structures are activated during SE and may also be involved in the subsequent epileptogenic process. Here we have investigated whether SE, induced in rats with pilocarpine and terminated after 40 min with diazepam, persistently modifies the intrinsic excitability of pyramidal neurons in the subiculum. Subicular slices were prepared from control and SE‐experienced rats (2–5 weeks after SE). In the control group, only 4% of the neurons fired bursts in response to intrasomatic, threshold‐straddling depolarizing current pulses (low‐threshold bursters). The remaining neurons either fired bursts in response to strong (3× threshold) depolarizations (35%; high‐threshold bursters) or fired in a completely regular mode (61%; nonbursters). In the SE‐experienced group, the fractions of low‐ and high‐threshold bursters markedly increased to 29% and 53%, respectively. This change in firing behaviour was associated with a marked increase in the size of the spike afterdepolarization, particularly in low‐threshold bursters. Experimental suppression of Ca 2+ currents selectively blocked low‐threshold bursting but did not affect high‐threshold bursting, suggesting that a dual Ca 2+ ‐ dependent and Ca 2+ ‐ independent mechanism controls bursting in these neurons. The persistent up‐regulation of intrinsic bursting in the subiculum, in concert with similar changes in the hippocampus, undoubtedly contributes to epileptogenesis following pilocarpine‐induced SE.