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Alcohol and Opioids Modulate Excitatory Inputs to the SCN.

William Purvines1,2, Valerie Vierkant1, Peyton Westbo1

  • 1Department of Neuroscience and Experimental Therapeutics, College of Medicine, Texas A&M University Health Science Center, Bryan, Texas 77807.

Biorxiv : the Preprint Server for Biology
|May 18, 2026
PubMed
Summary
This summary is machine-generated.

Alcohol and opioids alter brain rhythms by affecting glutamatergic input to the suprachiasmatic nucleus (SCN). This research identifies the SCN as a new target for depressants, impacting circadian regulation in substance use disorders.

Keywords:
AlcoholSCNSuprachiasmatic nucleus (SCN)circadian rhythmscircadian systemsdepressantsopioidssubstance use disorders

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Area of Science:

  • Neuroscience
  • Chronobiology
  • Pharmacology

Background:

  • Circadian rhythm disruption is common in substance use disorders.
  • The suprachiasmatic nucleus (SCN) is the brain's central circadian pacemaker.
  • Cellular mechanisms of depressant effects on the SCN are not well understood.

Purpose of the Study:

  • Investigate how alcohol and opioids affect glutamatergic transmission in the SCN.
  • Determine the impact of acute and chronic alcohol exposure on SCN function.
  • Explore opioid receptor-mediated modulation of SCN neuronal activity.

Main Methods:

  • Whole-cell patch clamp electrophysiology in brain slices.
  • Acute and chronic alcohol exposure paradigms.
  • Optogenetic stimulation and MOR agonist application.

Main Results:

  • Acute ethanol enhanced SCN firing rates; chronic exposure reduced glutamatergic drive.
  • Activation of MOR+ terminals bidirectionally modulated SCN firing.
  • MOR+ inputs formed functional glutamatergic synapses suppressed by MOR agonists.

Conclusions:

  • Alcohol and opioids modulate glutamatergic input to the SCN.
  • The SCN is a novel target for depressant substances.
  • Glutamatergic transmission in the SCN is a vulnerability in substance use-related circadian dysregulation.