Alcohol withdrawal and pain: Peripheral mechanisms join central circuits

Volker Neugebauer; Igor Ponomarev

doi:10.1016/j.neuron.2023.12.006

Alcohol withdrawal and pain: Peripheral mechanisms join central circuits

Neuron. 2024 Jan 3;112(1):1-3. doi: 10.1016/j.neuron.2023.12.006.

Authors

Volker Neugebauer¹, Igor Ponomarev²

Affiliations

¹ Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center (TTUHSC), Lubbock, TX, USA; Center of Excellence for Translational Neuroscience and Therapeutics, Texas Tech University Health Sciences Center (TTUHSC), Lubbock, TX, USA; Garrison Institute on Aging, Texas Tech University Health Sciences Center (TTUHSC), Lubbock, TX, USA. Electronic address: volker.neugebauer@ttuhsc.edu.
² Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center (TTUHSC), Lubbock, TX, USA; Center of Excellence for Translational Neuroscience and Therapeutics, Texas Tech University Health Sciences Center (TTUHSC), Lubbock, TX, USA.

PMID: 38176389
DOI: 10.1016/j.neuron.2023.12.006

Abstract

Negative affective aspects of alcohol withdrawal and pain involve converging brain circuits. In this issue of Neuron, Son et al.¹ identify a peripheral mechanism of an alcohol-withdrawal-induced headache-like condition, which is centered on mast-cell-specific receptor MrgprB2 activated by corticotropin-releasing factor (CRF) in dura mater to drive nociception.

Keywords: CRF; alcohol use disorder; corticotropin-releasing factor; headache; mast cells; neuroinflammation; nociception; pain.

MeSH terms

Alcoholism*
Corticotropin-Releasing Hormone
Humans
Pain
Receptors, Corticotropin-Releasing Hormone / physiology
Substance Withdrawal Syndrome* / psychology

Substances

Receptors, Corticotropin-Releasing Hormone
Corticotropin-Releasing Hormone

Abstract

MeSH terms

Substances

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