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  • Title: Dendritic Na+ current inactivation can increase cell excitability by delaying a somatic depolarizing afterpotential.
    Author: Fernandez FR, Mehaffey WH, Turner RW.
    Journal: J Neurophysiol; 2005 Dec; 94(6):3836-48. PubMed ID: 16120659.
    Abstract:
    Many central neurons support active dendritic spike backpropagation mediated by voltage-gated currents. Active spikes in dendrites have been shown capable of providing feedback to the soma to influence somatic excitability and firing dynamics through a depolarizing afterpotential (DAP). In pyramidal cells of the electrosensory lobe of weakly electric fish, Na(+) spikes in dendrites undergo a frequency-dependent broadening that enhances the DAP to increase somatic firing frequency. We use a combination of dynamical analysis and electrophysiological recordings to demonstrate that spike broadening in dendrites is primarily caused by a cumulative inactivation of dendritic Na(+) current. We further show that a reduction in dendritic Na(+) current increases excitability by decreasing the interspike interval and promoting burst firing. This process arises when inactivation of dendritic Na(+) current shifts the latency of the dendritic spike to delay the arrival of the DAP sufficiently to increase its impact on somatic membrane potential despite a reduction in dendritic excitability. Furthermore, the relationship between dendritic Na(+) current density and somatic excitability is nonmonotonic, as intermediate levels of dendritic Na(+) current exert the greatest excitatory influence. These results reveal that temporal shifts in dendritic spike firing provide a novel means for backpropagating spikes to influence the final output of a cell.
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