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Intracellular recordings in thalamic neurones during spontaneous spike and wave discharges in rats with absence epilepsy
Author(s) -
Pinault Didier,
Leresche Nathalie,
Charpier Stéphane,
Deniau JeanMichel,
Marescaux Christian,
Vergnes Marguerite,
Crunelli Vincenzo
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.449bn.x
Subject(s) - excitatory postsynaptic potential , depolarization , inhibitory postsynaptic potential , neuroscience , intracellular , tonic (physiology) , hyperpolarization (physics) , bursting , epilepsy , spike and wave , chemistry , electrophysiology , extracellular , postsynaptic potential , spike potential , biophysics , biology , receptor , biochemistry , stereochemistry , nuclear magnetic resonance spectroscopy
1 In vivo extracellular and intracellular recordings were performed from thalamocortical (TC) neurones in a genetic model of absence epilepsy (genetic absence epilepsy rats from Strasbourg) during spontaneous spike and wave discharges (SWDs). 2 Extracellularly recorded single units ( n = 14 ) fired either a single action potential or a high frequency burst of up to three action potentials, concomitantly with the spike component of the spike‐wave complex. 3 Three main events characterized the intracellular activity of twenty‐six out of twenty‐eight TC neurones during SWDs: a small amplitude tonic hyperpolarization that was present throughout the SWD, rhythmic sequences of EPSP/IPSPs occurring concomitantly with the spike‐wave complexes, and a small tonic depolarization at the end of the SWD. The rhythmic IPSPs, but not the tonic hyperpolarization, were mediated by activation of GABA A receptors since they reversed in polarity at ‐68 mV and appeared as depolarizing events when recording with KCl‐filled electrodes. 4 The intracellular activity of the remaining two TC neurones consisted of rhythmic low threshold Ca 2+ potentials, with a few EPSP/IPSP sequences present at the start of the SWD. 5 These results obtained in a well‐established genetic model of absence epilepsy do not support the hypothesis that the intracellular activity of TC neurones during SWDs involves rhythmic sequences of GABA B IPSPs and low threshold Ca 2+ potentials.