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Acute effect of carbamazepine on corticothalamic 5–9‐ H z and thalamocortical spindle (10–16‐ H z) oscillations in the rat
Author(s) -
Zheng Thomas W.,
O'Brien Terence J.,
Kulikova Sofya P.,
Reid Christopher A.,
Morris Margaret J.,
Pinault Didier
Publication year - 2014
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 - 10.1111/ejn.12441
Subject(s) - neuroscience , depolarization , reticular connective tissue , electroencephalography , thalamus , thalamic reticular nucleus , sleep spindle , chemistry , physics , slow wave sleep , biophysics , biology , anatomy
A major side effect of carbamazepine ( CBZ ), a drug used to treat neurological and neuropsychiatric disorders, is drowsiness, a state characterized by increased slow‐wave oscillations with the emergence of sleep spindles in the electroencephalogram ( EEG ). We conducted cortical EEG and thalamic cellular recordings in freely moving or lightly anesthetized rats to explore the impact of CBZ within the intact corticothalamic ( CT )–thalamocortical ( TC ) network, more specifically on CT 5–9‐Hz and TC spindle (10–16‐Hz) oscillations. Two to three successive 5–9‐Hz waves were followed by a spindle in the cortical EEG . A single systemic injection of CBZ (20 mg/kg) induced a significant increase in the power of EEG 5–9‐Hz oscillations and spindles. Intracellular recordings of glutamatergic TC neurons revealed 5–9‐Hz depolarizing wave–hyperpolarizing wave sequences prolonged by robust, rhythmic spindle‐frequency hyperpolarizing waves. This hybrid sequence occurred during a slow hyperpolarizing trough, and was at least 10 times more frequent under the CBZ condition than under the control condition. The hyperpolarizing waves reversed at approximately −70 mV, and became depolarizing when recorded with KC l‐filled intracellular micropipettes, indicating that they were GABA A receptor‐mediated potentials. In neurons of the GABA ergic thalamic reticular nucleus, the principal source of TC GABA ergic inputs, CBZ augmented both the number and the duration of sequences of rhythmic spindle‐frequency bursts of action potentials. This indicates that these GABA ergic neurons are responsible for the generation of at least the spindle‐frequency hyperpolarizing waves in TC neurons. In conclusion, CBZ potentiates GABA A receptor‐mediated TC spindle oscillations. Furthermore, we propose that CT 5–9‐Hz waves can trigger TC spindles.