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This Article Full Text Full Text (PDF) Supplemental data All Versions of this Article: 578/2/527    most recent jphysiol.2006.123463v1 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 Zsiros, V. Articles by Maccaferri, G. Search for Related Content PubMed PubMed Citation Articles by Zsiros, V. Articles by Maccaferri, G. Related Collections Neuroscience

¹ Department of Physiology, Feinberg School of Medicine
² Institute for Neuroscience, Northwestern University, Chicago, IL 60611, USA

The integration of synaptic signalling in the mammalian hippocampus underlies higher cognitive functions such as learning and memory. We have studied the gap junction-mediated cell-to-cell and network propagation of GABA_A receptor-mediated events in stratum lacunosum moleculare interneurons of the rat hippocampus. Propagated events were identified both in voltage- and current-clamp configurations. After blockade of ionotropic excitatory synaptic transmission, voltage-clamp recordings with chloride-loaded electrodes (predicted GABA_A receptor reversal potential: 0 mV) at –15 mV revealed the unexpected presence of spontaneous events of opposite polarities. Inward events were larger and kinetically faster when compared to outward currents. Both types of events were blocked by gabazine, but only outward currents were significantly affected by the gap junction blocker carbenoxolone, indicating that outward events originated in electrically coupled neurons. These results were in agreement with computational modelling showing that propagated events were modulated in size and shape by their relative distance to the gap junction site. Paired recordings from electrically coupled interneurons performed with high- and low-chloride pipettes (predicted GABA_A receptor reversal potentials: 0 mV and –80 mV, respectively) directly demonstrated that depolarizing postsynaptic events could propagate to the cell recorded with the low-chloride solution. Cell-to-cell propagation was abolished by carbenoxolone, and was not observed in uncoupled pairs. Application of 4-aminopyridine on slices resulted in spontaneous network activation of interneurons, which was driven by excitatory GABA_A receptor-mediated input. Population activity was greatly depressed by carbenoxolone, suggesting that propagation of depolarizing synaptic GABAergic potentials may be a critical determinant of interneuronal synchronous bursting in the hippocampus.

(Received 25 October 2006; accepted after revision 10 November 2006; first published online 16 November 2006)
Corresponding author G. Maccaferri: Department of Physiology, Northwestern University, Feinberg Medical School, 303 E Chicago Ave, Tarry Blg Rm 5-707 M211, Chicago, IL 60611, USA. Email: g-maccaferri{at}northwestern.edu

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