RT Journal Article
SR Electronic
T1 Multiple Conductances Cooperatively Regulate Spontaneous Bursting in Mouse Olfactory Bulb External Tufted Cells
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1625
OP 1639
DO 10.1523/JNEUROSCI.3906-07.2008
VO 28
IS 7
A1 Shaolin Liu
A1 Michael T. Shipley
YR 2008
UL http://www.jneurosci.org/content/28/7/1625.abstract
AB External tufted (ET) cells are juxtaglomerular neurons that spontaneously generate bursts of action potentials, which persist when fast synaptic transmission is blocked. The intrinsic mechanism of this autonomous bursting is unknown. We identified a set of voltage-dependent conductances that cooperatively regulate spontaneous bursting: hyperpolarization-activated inward current (Ih), persistent Na+ current (INaP), low-voltage-activated calcium current (IL/T) mediated by T- and/or L-type Ca2+ channels, and large-conductance Ca2+-dependent K+ current (IBK). Ih is important in setting membrane potential and depolarizes the cell toward the threshold of INaP and IT/L, which are essential to generate the depolarizing envelope that is crowned by a burst of action potentials. Action potentials depolarize the membrane and induce Ca2+ influx via high-voltage-activated Ca2+ channels (IHVA). The combined depolarization and increased intracellular Ca2+ activates IBK, which terminates the burst by hyperpolarizing the membrane. Hyperpolarization activates Ih and the cycle is regenerated. A novel finding is the role of L-type Ca2+ channels in autonomous ET cells bursting. A second novel feature is the role of BK channels, which regulate burst duration. IL and IBK may go hand-in-hand, the slow inactivation of IL requiring IBK-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.