# Attenuation of microglial aryl hydrocarbon receptor alters astrocyte activation and chronic pain sensitization in aging

## TL;DR

This study shows that reduced AHR in aged mice's microglia increases astrocyte activation and chronic pain.

## Contribution

The novel finding is that microglial AHR regulates astrocyte activation and chronic pain in aging.

## Key findings

- AHR expression in spinal dorsal horn microglia is significantly lower in aged mice.
- Reduced microglial AHR enhances astrocyte activation and inflammation.
- Lower AHR in aged mice contributes to prolonged pain sensitization.

## Abstract

This study aims to examine differences in aryl hydrocarbon receptor (AHR) expression between microglia in aged and adult mice and to investigate the impact of microglial AHR attenuation on chronic pain sensitization. Immunofluorescence staining was performed to assess AHR expression in microglia. BV2 microglial cells were treated with lipopolysaccharides (LPS), the AHR agonist FICZ, and the AHR antagonist CH223191. The resulting supernatant was used to culture C8-DIA astrocytes, and inflammatory factor levels were quantified using quantitative real-time polymerase chain reaction. AHR expression in spinal dorsal horn microglia was significantly lower in aged mice compared to adult mice. Furthermore, microglial AHR expression was found to regulate astrocyte activation. AHR expression in spinal dorsal horn microglia is markedly reduced in aged mice. Activated microglia with diminished AHR expression induce astrocytes more strongly and enhance astrocyte-mediated inflammation, contributing to prolonged hyperalgesia in aged mice.