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This Article Full Text Full Text (PDF) All Versions of this Article: 100/2/576    most recent 90263.2008v1 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 ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Dibattista, M. Articles by Menini, A. PubMed PubMed Citation Articles by Dibattista, M. Articles by Menini, A.

Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels in Mouse Vomeronasal Sensory Neurons

¹Sector of Neurobiology, International School for Advanced Studies, Scuola Internazionale di Studi Superiori Avanzati (SISSA), Trieste; ²Italian Institute of Technology, SISSA Unit, Trieste; and ³Section of Physiology, Department of Neuroscience, University of Parma, Parma, Italy

Submitted 4 February 2008; accepted in final form 21 May 2008

Hyperpolarization-activated currents (I_h) are present in several neurons of the central and peripheral nervous system. However, I_h in neurons of the vomeronasal organ (VNO) is not well characterized. We studied the properties of I_h in sensory neurons from acute slices of mouse VNO. In voltage-clamp studies, I_h was identified by the characteristic kinetics of activation, voltage dependence, and blockage by Cs⁺ or ZD-7288, two blockers of the I_h. Forskolin, an activator of adenylyl cyclase, shifted the activation curve for I_h to less negative potentials. A comparison of I_h properties in VNO neurons with those of heterologously expressed hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, together with RT-PCR experiments in VNO, indicate that I_h is caused by HCN2 and/or HCN4 subunits. In current-clamp recordings, blocking I_h with ZD-7288 induced a hyperpolarization of 5.1 mV, an increase in input resistance, a decrease in the sensitivity to elicit action potentials in response to small current injections, and did not modify the frequency of action potentials elicited by a large current injection. It has been shown that in VNO neurons some pheromones induce a decrease in cAMP concentration, but the physiological role of cAMP is unknown. After application of blockers of adenylyl cyclase, we measured a hyperpolarization of 5.1 mV in 11 of 14 neurons, suggesting that basal levels of cAMP could modulate the resting potential. In conclusion, these results show that mouse VNO neurons express HCN2 and/or HCN4 subunits and that I_h contributes to setting the resting membrane potential and to increase excitability at stimulus threshold.