SK channel regulation of dendritic excitability and dendrodendritic inhibition in the olfactory bulb

Brady J. Maher, Gary Westbrook

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

Small-conductance calcium-activated potassium channels (SK) regulate dendritic excitability in many neurons. In the olfactory bulb, regulation of backpropagating action potentials and dendrodendritic inhibition depend on the dendritic excitability of mitral cells. We report here that SK channel currents are present in mitral cells but are not detectable in granule cells in the olfactory bulb. In brain slices from PND 14-21 mice, long step depolarizations (100 ms) in the mitral cell soma evoked a cadmium- and apamin-sensitive outward SK current lasting several hundred milliseconds. Block of the SK current unmasked an inward N-methyl-D-aspartate (NMDA) autoreceptor current due to glutamate released from mitral cell dendrites. In low extracellular Mg 2+ (100 μM), brief step depolarizations (2 ms) evoked an apamin-sensitive current that was reduced by D,L-2-amino-5-phosphonopentanoic acid. In current-clamp, block of SK channels increased action potential firing in mitral cells as well as dendrodendritic inhibition. Our results indicate that SK channels can be activated either by calcium channels or NMDA channels in mitral cell dendrites, providing a mechanism for local control of dendritic excitability.

Original languageEnglish (US)
Pages (from-to)3743-3750
Number of pages8
JournalJournal of Neurophysiology
Volume94
Issue number6
DOIs
StatePublished - Dec 2005

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Olfactory Bulb
Apamin
N-Methylaspartate
Dendrites
Action Potentials
Small-Conductance Calcium-Activated Potassium Channels
2-Amino-5-phosphonovalerate
Autoreceptors
Carisoprodol
Calcium Channels
Cadmium
Glutamic Acid
Neurons
Brain

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

SK channel regulation of dendritic excitability and dendrodendritic inhibition in the olfactory bulb. / Maher, Brady J.; Westbrook, Gary.

In: Journal of Neurophysiology, Vol. 94, No. 6, 12.2005, p. 3743-3750.

Research output: Contribution to journalArticle

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