Related Experiment Video
Updated: May 19, 2026
09:29
Investigating Drivers of Antireward in Addiction Behavior with Anatomically Specific Single-Cell Gene Expression Methods
Published on: August 4, 2022
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
Summary
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.
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.
Related Concept Videos
01:27CNS Depressants: Alcohol and Nicotine
Ethanol, a clear colorless alcohol, has been consumed by humans for millennia, but its effects on the body are far from benign. At lower doses, it induces decreased inhibitions and loquaciousness, leading to its social appeal. However, it can cause severe consequences at higher doses, such as coma and respiratory depression, due to its zero-order elimination kinetics. Chronic ethanol abuse wreaks havoc on multiple organ systems, particularly the CNS and the liver. Abrupt cessation of ethanol...
01:22Opioid Receptors: Overview
Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2, D-Pen5]-enkephalin or DPDPE for...
01:25Analgesia and Pain Management
Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
01:29Excitatory and Inhibitory Effects of Neurotransmitters
When an action potential reaches the presynaptic axon terminal, it releases neurotransmitters from the neuron into the synaptic cleft at a chemical synapse. The released neurotransmitter can be excitatory or inhibitory. The critical criteria commonly used to determine whether a molecule is a neurotransmitter at a chemical synapse are the molecule's presence in the presynaptic neuron. Second, its release is in response to strong presynaptic depolarization. And lastly, the presence of specific...
01:28Depressants
Depressant drugs, including alcohol and sedative-hypnotics, diminish central nervous system activity by enhancing the action of gamma-aminobutyric acid (GABA), a neurotransmitter that reduces brain activity and promotes relaxation. These substances can have various therapeutic uses but also pose significant risks, especially when misused or combined.
Alcohol is a common depressant that can induce a sense of relaxation and reduced inhibition at low doses. Contrary to its occasional...
Alcohol is a common depressant that can induce a sense of relaxation and reduced inhibition at low doses. Contrary to its occasional...
01:24CNS Stimulants: Cocaine, Amphetamines and Cannabinoids
CNS stimulants, such as cocaine, amphetamines, and cannabinoids, have varying structures and mechanisms of action that lead to different therapeutic effects and side effects. Cocaine, with its molecular formula C17H21NO4, is a tropane alkaloid and a tertiary amino compound. It has two chemical forms: the hydrochloride salt and the "freebase." The former is in powder form, while the latter involves removing the hydrochloride salt to create a form that can be smoked. Cocaine exerts its effects by...