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We identified a set of voltage-dependent conductances that cooperatively regulate spontaneous bursting: hyperpolarization-activated inward current (<jats:italic>I<\/jats:italic><jats:sub>h<\/jats:sub>), persistent Na<jats:sup>+<\/jats:sup>current (<jats:italic>I<\/jats:italic><jats:sub>NaP<\/jats:sub>), low-voltage-activated calcium current (<jats:italic>I<\/jats:italic><jats:sub>L\/T<\/jats:sub>) mediated by T- and\/or L-type Ca<jats:sup>2+<\/jats:sup>channels, and large-conductance Ca<jats:sup>2+<\/jats:sup>-dependent K<jats:sup>+<\/jats:sup>current (<jats:italic>I<\/jats:italic><jats:sub>BK<\/jats:sub>).<jats:italic>I<\/jats:italic><jats:sub>h<\/jats:sub>is important in setting membrane potential and depolarizes the cell toward the threshold of<jats:italic>I<\/jats:italic><jats:sub>NaP<\/jats:sub>and<jats:italic>I<\/jats:italic><jats:sub>T\/L<\/jats:sub>, which are essential to generate the depolarizing envelope that is crowned by a burst of action potentials. Action potentials depolarize the membrane and induce Ca<jats:sup>2+<\/jats:sup>influx via high-voltage-activated Ca<jats:sup>2+<\/jats:sup>channels (<jats:italic>I<\/jats:italic><jats:sub>HVA<\/jats:sub>). The combined depolarization and increased intracellular Ca<jats:sup>2+<\/jats:sup>activates<jats:italic>I<\/jats:italic><jats:sub>BK<\/jats:sub>, which terminates the burst by hyperpolarizing the membrane. Hyperpolarization activates<jats:italic>I<\/jats:italic><jats:sub>h<\/jats:sub>and the cycle is regenerated. A novel finding is the role of L-type Ca<jats:sup>2+<\/jats:sup>channels in autonomous ET cells bursting. A second novel feature is the role of BK channels, which regulate burst duration.<jats:italic>I<\/jats:italic><jats:sub>L<\/jats:sub>and<jats:italic>I<\/jats:italic><jats:sub>BK<\/jats:sub>may go hand-in-hand, the slow inactivation of<jats:italic>I<\/jats:italic><jats:sub>L<\/jats:sub>requiring<jats:italic>I<\/jats:italic><jats:sub>BK<\/jats:sub>-dependent hyperpolarization to deactivate inward conductances and terminate the burst. ET cells receive monosynaptic olfactory nerve input and drive the major inhibitory interneurons of the glomerular circuit. Modulation of the conductances identified here can regulate burst frequency, duration, and spikes per burst in ET cells and thus significantly shape the impact of glomerular circuits on mitral and tufted cells, the output channels of the olfactory bulb.<\/jats:p>","DOI":"10.1523\/jneurosci.3906-07.2008","type":"journal-article","created":{"date-parts":[[2008,2,13]],"date-time":"2008-02-13T17:30:20Z","timestamp":1202923820000},"page":"1625-1639","source":"Crossref","is-referenced-by-count":78,"title":["Multiple Conductances Cooperatively Regulate Spontaneous Bursting in Mouse Olfactory Bulb External Tufted Cells"],"prefix":"10.1523","volume":"28","author":[{"given":"Shaolin","family":"Liu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael 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