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Emergence of disinhibition‐induced synchrony in the CA3 region of the guinea pig hippocampus in vitro
Author(s) -
Cohen Ivan,
Huberfeld Gilles,
Miles Richard
Publication year - 2006
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 - 10.1113/jphysiol.2005.097899
Subject(s) - excitatory postsynaptic potential , inhibitory postsynaptic potential , neuroscience , hippocampal formation , population , hippocampus , population spike , biology , chemistry , medicine , environmental health
Suppressing inhibition mediated by GABA A 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 GABA A 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 GABA A receptor antagonists. Intracellular records suggest that inhibitory signalling mediated by GABA B receptors contributes to the emergence of this activity. States of partial synchrony in the CA3 region exposed to GABA A receptor antagonists therefore depend on alternating periods of firing, presumably dependent on excitatory synaptic mechanisms, and silence, mediated in part by the activation of GABA B receptors.

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