Table of Contents

This Week in The Journal

A Circuit for the Combined Effects of Chronic Pain and Binge Alcohol Consumption

Yuexi Yin, David L. Haggerty, Shudi Zhou, Brady K. Atwood, and Patrick L. Sheets

(see article e1287232024)

There is strong comorbidity between chronic pain and alcohol use disorder (AUD), but whether the two diseases share common mechanisms of action is unclear. The anterior insular cortex (AIC) is involved in chronic pain and AUD, but it remains unknown if there are circuit-specific changes when both simultaneously occur. Yin, Haggerty et al. explored this in mice using both cellular and behavioral methodology. They modeled binge-like alcohol consumption using the Drinking-in-the-Dark (DID) paradigm and induced chronic pain using spared nerve injury (SNI). They found that SNI male (but not female) mice with no prior exposure to alcohol consumed less alcohol than control mice during DID. These mice had increased excitability in a subset of AIC neurons projecting to the dorsolateral striatum (DLS). Cellular recordings revealed an increased frequency of excitatory inputs to these AIC–DLS neurons. When SNI male mice were exposed to alcohol prior to injury, they consumed similar amounts of alcohol postinjury as control mice. The findings of this study fill many gaps in knowledge on circuit mechanisms underlying the converging effects of chronic pain and alcohol drinking by revealing a pivotal role of AIC–DLS neuron activity in this interaction.

Representative heatmaps for a mouse during an alcohol conditioned place preference assay. The top heatmap is the baseline session and the bottom heatmap is the test session following conditioning. Both sham and SNI mice showed increased alcohol preference during the test session as compared with baseline.

New Structural Measurement for Age- and Alzheimer's-Associated Cognitive Decline

Samira A. Maboudian, Ethan H. Willbrand, William J. Jagust, and Kevin S. Weiner

(see article e1714232024)

Our cortical brain structure undergoes drastic changes as we experience cognitive decline through aging or in disease states such as Alzheimer's disease (AD). Emerging evidence suggests that sulci may be extra susceptible to age- and AD-related deterioration. The posteromedial cortex (PMC) is thought to have the most extreme susceptibility, but the vulnerability of smaller, shallower sulci remains unexplored. In this issue, Maboudian et al. used magnetic resonance imaging to measure structural differences in manually defined tertiary sulci of 216 human study participants during aging and in AD. They found more age- and AD-related thinning of small, shallow sulci, including two previously unidentified sulci, than in the larger PMC sulci. The authors used a computational model based on data from the Alzheimer's Disease Neuroimaging Initiative database to discover that atrophy of a portion of the sulci, including the ones they newly identified, was most strongly associated with cognitive decline as measured by memory and executive function scores. These novel measurements provide more insight into age- and AD-related structural changes of the brain, which can vary significantly between individuals and may contribute to individual differences in cognitive decline.

Footnotes

  • This Week in The Journal was written by Paige McKeon

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