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Details

Autor(en) / Beteiligte
Titel
Complementary Tuning of Na+ and K+ Channel Gating Underlies Fast and Energy-Efficient Action Potentials in GABAergic Interneuron Axons
Ist Teil von
  • Neuron (Cambridge, Mass.), 2018-04, Vol.98 (1), p.156-165.e6
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2018
Link zum Volltext
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
  • Fast-spiking, parvalbumin-expressing GABAergic interneurons (PV+-BCs) express a complex machinery of rapid signaling mechanisms, including specialized voltage-gated ion channels to generate brief action potentials (APs). However, short APs are associated with overlapping Na+ and K+ fluxes and are therefore energetically expensive. How the potentially vicious combination of high AP frequency and inefficient spike generation can be reconciled with limited energy supply is presently unclear. To address this question, we performed direct recordings from the PV+-BC axon, the subcellular structure where active conductances for AP initiation and propagation are located. Surprisingly, the energy required for the AP was, on average, only ∼1.6 times the theoretical minimum. High energy efficiency emerged from the combination of fast inactivation of Na+ channels and delayed activation of Kv3-type K+ channels, which minimized ion flux overlap during APs. Thus, the complementary tuning of axonal Na+ and K+ channel gating optimizes both fast signaling properties and metabolic efficiency. •Brief AP duration and high AP frequency in PV+-BCs may imply high metabolic cost•Energy for AP generation in PV+-BC axons is only 1.6 times the theoretical minimum•Fast Nav inactivation and delayed Kv3 activation maximize AP energy efficiency•Tuning of Nav–Kv3 gating optimizes fast signaling and energetics in interneurons Hu et al. demonstrate that action potentials in parvalbumin-expressing GABAergic interneuron axons are energetically efficient, which is highly unexpected given their brief duration. High energy efficiency emerges from the combination of fast inactivation of voltage-gated Na+ channels and delayed activation of Kv3 channels in the axon.

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