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J Physiol Volume 570, Number 3, 583-594, February 1, 2006 DOI: 10.1113/jphysiol.2005.097899
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Emergence of disinhibition-induced synchrony in the CA3 region of the guinea pig hippocampus in vitro

Ivan Cohen1, Gilles Huberfeld1 and Richard Miles1

1 INSERM U739, CHU Pité-Salpêtrière, UPMC, 105 bd de l'Hôpital, 75013 Paris, France

Suppressing inhibition mediated by GABAA receptors induces rhythmic bursts of synchronous firing in the CA3 region of the hippocampus. Extracellular and intracellular records were made from guinea pig hippocampal slices to examine the emergence of this synchrony. We found that application of GABAA receptor antagonists initiated a sequence of changes in the activity of the CA3 neuronal population. First, the frequency of firing detected in multiunit records increased. Then, firing began to oscillate with increases followed by decreases in firing that occurred at intervals of 0.5–2 s. The coherence of the rhythmic activity at a single site increased with time, and discharges at distant sites in the CA3 region became correlated. Fluctuations in firing were associated with extracellular field potentials. Finally, epileptiform events associated with large field potentials began to recur at intervals of 5–10 s. The onset of fully synchronous events was sudden and correlated with a large increase in the amplitude of the field potential. Thus the CA3 population can express states of partial population synchrony preceding the onset of epileptiform discharges. A similar activity was induced and maintained by applying low doses of GABAA receptor antagonists. Intracellular records suggest that inhibitory signalling mediated by GABAB receptors contributes to the emergence of this activity. States of partial synchrony in the CA3 region exposed to GABAA receptor antagonists therefore depend on alternating periods of firing, presumably dependent on excitatory synaptic mechanisms, and silence, mediated in part by the activation of GABAB receptors.

(Received 31 August 2005; accepted after revision 30 November 2005; first published online 1 December 2005)
Corresponding author I. Cohen: Baylor College of Medicine, Neurology Department, Room NB-220, 1 Baylor Plaza, Houston, TX 77030, USA. Email: icohen{at}bcm.tmc.edu




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