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This Article Full Text Full Text (PDF) All Versions of this Article: 566/3/885    most recent jphysiol.2005.088708v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Benini, R. Articles by Avoli, M. Search for Related Content PubMed PubMed Citation Articles by Benini, R. Articles by Avoli, M.

¹ Montreal Neurological Institute and Departments of Neurology & Neurosurgery, and of Physiology, McGill University, Montreal, QC, H3A 2B4, Canada
² Dipartimento di Fisiologia Umana e Farmacologia, Università di Roma ‘La Sapienza’, 00185 Rome, Italy

Evidence obtained from human epileptic tissue maintained in vitro indicates that the subiculum may play a crucial role in initiating epileptiform discharges in patients with mesial temporal lobe epilepsy. Hence, we used rat hippocampus–entorhinal cortex (EC) slices to identify the role of subiculum in epileptiform synchronization during bath application of 4-aminopyridine (4AP, 50 µM). In these slices, fast CA3-driven interictal-like events were restricted to the hippocampal CA3/CA1 areas and failed to propagate to the EC where slow interictal-like and ictal-like epileptiform discharges were recorded. However, antagonizing GABA_A receptors with picrotoxin (50 µM) made CA3-driven interictal activity spread to EC. Sequential field potential analysis along the CA3–CA1–subiculum axis revealed that the amplitude of CA3-driven interictal discharges recorded in the presence of 4AP only diminished within the subiculum. Furthermore, CA1 electrical stimulation under control conditions elicited little or no subicular activation and never any response in EC; in contrast, robust subicular discharges that spread to EC could be evoked after picrotoxin. Intracellular recordings indicated that potentiation by picrotoxin was associated with blockade of hyperpolarizing IPSPs in subicular cells. Finally, when surgically isolated from adjacent structures, the subiculum generated low-amplitude synchronous discharges that corresponded to an intracellular hyperpolarization–depolarization sequence, were resistant to glutamatergic antagonists, and represented the activity of synchronized interneuronal networks. Bath application of picrotoxin abolished these 4AP-induced events and in their place robust network bursting occurred. In conclusion, our study demonstrates that the subiculum plays a powerful gating role on hippocampal output activity. This function depends on GABA_A receptor-mediated inhibition and controls hippocampal–parahippocampal interactions that are known to modulate limbic seizures.

(Received 15 April 2005; accepted after revision 31 May 2005; first published online 2 June 2005)
Corresponding author M. Avoli: 3801 University, room 794, Montreal, QC, Canada H3A 2B4. Email: massimo.avoli{at}mcgill.ca

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