Abstract

Summary

Somatostatin (SST) signaling in the suprachiasmatic nucleus acts as a brake on circadian plasticity, with SST-knockout mice showing enhanced behavioral and molecular responses to photoperiod changes, jet lag, and constant light. These findings reveal a sex-differentiated peptide mechanism in the central clock that could inform understanding of individual differences in circadian entrainment and light sensitivity.
Abstract

Key Findings

  • Sst-/- mice displayed enhanced circadian responses to light, including increased behavioral plasticity under photoperiod changes, jet lag protocols, and constant light conditions.
  • Elimination of SST signaling removed sex differences in photic responses, primarily due to increased circadian plasticity in males.
  • Sst-/- mice showed an increase in the number of retinorecipient neurons in the SCN core expressing SST receptors capable of resetting the molecular clock.
  • Loss of SST modulated SCN photoperiodic encoding, network after-effects, and intercellular synchrony in a sex-specific manner.
  • Cell-fate mapping provided evidence that SCN SST expression is regulated by light via de novo Sst gene activation.
Categories

Categories

Sleep & Circadian Health: Investigates how somatostatin signaling regulates circadian clock function, photoperiodic encoding, and behavioral responses to light including jet lag and constant light conditions.
The Science of Light: Examines SCN circuit mechanisms underlying photic processing, including retinorecipient neuron populations and peptide signaling that modulates circadian entrainment in a sex-specific manner.
Authors

Author(s)

DAM Joye
Publication Date

Publication Year

2022
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