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This Article Full Text Full Text (PDF) All Versions of this Article: 102/2/974    most recent 00060.2009v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science 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 Web of Science (1) Google Scholar Articles by Tovar, K. R. Articles by Westbrook, G. L. PubMed PubMed Citation Articles by Tovar, K. R. Articles by Westbrook, G. L.

Direct Actions of Carbenoxolone on Synaptic Transmission and Neuronal Membrane Properties

Vollum Institute, Oregon Health and Science University, Portland, Oregon

Submitted 21 January 2009; accepted in final form 10 June 2009

The increased appreciation of electrical coupling between neurons has led to many studies examining the role of gap junctions in synaptic and network activity. Although the gap junctional blocker carbenoxolone (CBX) is effective in reducing electrical coupling, it may have other actions as well. To study the non–gap junctional effects of CBX on synaptic transmission, we recorded from mouse hippocampal neurons cultured on glial micro-islands. This recording configuration allowed us to stimulate and record excitatory postsynaptic currents (EPSCs) or inhibitory postsynaptic currents (IPSCs) in the same neuron or pairs of neurons. CBX irreversibly reduced evoked -amino-3-hydroxy-5-methyl-4-isoxazole-proprionic acid (AMPA) receptor–mediated EPSCs. Consistent with a presynaptic site of action, CBX had no effect on glutamate-evoked whole cell currents and increased the paired-pulse ratio of AMPA and N-methyl-D-aspartate (NMDA) receptor–mediated EPSCs. CBX also reversibly reduced GABA_A receptor–mediated IPSCs, increased the action potential width, and reduced the action potential firing rate. Our results indicate CBX broadly affects several neuronal membrane conductances independent of its effects on gap junctions. Thus effects of carbenoxolone on network activity cannot be interpreted as resulting from specific block of gap junctions.

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