DESCRIPTION:

QTL associated with delta power in slow-wave sleep 3. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (34137861)

LABEL:

QTL-Dps3-Mouse-Chr 17

SCORE TYPE:

Binary

DATE ADDED:

2012-04-02

DATE UPDATED:

2020-05-06

SPECIES:

URI:

http://www.informatics.jax.org/searches/accession_report.cgi?id=MGI:2136108

AUTHORS:

Franken P, Chollet D, Tafti M

TITLE:

The homeostatic regulation of sleep need is under genetic control.

JOURNAL:

The Journal of neuroscience : the official journal of the Society for Neuroscience Apr 2001, Vol 21, pp. 2610-21

ABSTRACT:

Delta power, a measure of EEG activity in the 1-4 Hz range, in slow-wave sleep (SWS) is in a quantitative and predictive relationship with prior wakefulness. Thus, sleep loss evokes a proportional increase in delta power, and excess sleep a decrease. Therefore, delta power is thought to reflect SWS need and its underlying homeostatically regulated recovery process. The neurophysiological substrate of this process is unknown and forward genetics might help elucidate the nature of what is depleted during wakefulness and recovered during SWS. We applied a mathematical method that quantifies the relationship between the sleep-wake distribution and delta power to sleep data of six inbred mouse strains. The results demonstrated that the rate at which SWS need accumulated varied greatly with genotype. This conclusion was confirmed in a "dose-response" study of sleep loss and changes in delta power; delta power strongly depended on both the duration of prior wakefulness and genotype. We followed the segregation of the rebound of delta power after sleep deprivation in 25 BXD recombinant inbred strains by quantitative trait loci (QTL) analysis. One "significant" QTL was identified on chromosome 13 that accounted for 49% of the genetic variance in this trait. Interestingly, the rate at which SWS need decreases did not vary with genotype in any of the 31 inbred strains studied. These results demonstrate, for the first time, that the increase of SWS need is under a strong genetic control, and they provide a basis for identifying genes underlying SWS homeostasis. PUBMED: 11306614
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