Increased γ- and decreased δ-oscillations in a mouse deficient for a potassium channel expressed in fast-spiking interneurons

Rolf H. Joho, Chi Shun Ho, Gerald A. Marks

Research output: Contribution to journalArticlepeer-review

68 Scopus citations

Abstract

Kv3.1 is a voltage-gated, fast activating/deactivating potassium (K+) channel with a high-threshold of activation and a large unit conductance. Kv3.1 K+ channels are expressed in fast- spiking, parvalbumin-containing interneurons in cortex, hippocampus, striatum, the thalamic reticular nucleus (TRN), and in several nuclei of the brain stem. A high density of Kv3.1 channels contributes to short-duration action potentials, fast afterhyperpolarizations, and brief refractory periods enhancing the capability in these neurons for high-frequency firing. Kv3.1 K+ channel expression 'm the TRN and cortex also suggests a role in thalamocortical and cortical function. Here we show that fast gamma and slow delta oscillations recorded from the somatomotor cortex are altered in the freely behaving Kv3.1 mutant mouse. Electroencephalographic (EEG) recordings from homozygous Kv3.1(-/-) mice show a three- to fourfold increase in both absolute and relative spectral power in the gamma frequency range (20-60 Hz). In contrast, Kv3.1-deficient mice have a 20-50% reduction of power in the slow delta range (2-3 Hz). The increase in gamma power is most prominent during waking in the 40- to 55-Hz range, whereas the decrease in delta power occurs equally across all states of arousal. Our findings suggest that Kv3.1-expressing neurons are involved in the generation and maintenance of cortical fast gamma and slow delta oscillations. Hence the Kv3.1-mutant mouse could serve as a model to study the generation and maintenance of fast gamma and slow delta rhythms and their involvement in behavior and cognition.

Original languageEnglish (US)
Pages (from-to)1855-1864
Number of pages10
JournalJournal of neurophysiology
Volume82
Issue number4
DOIs
StatePublished - 1999

ASJC Scopus subject areas

  • General Neuroscience
  • Physiology

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