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Neurons and Astrocytes in Ventrolateral Periaqueductal Gray Contribute to Restraint Water Immersion Stress-induced Gastric Mucosal Damage via the ERK1/2 Signaling Pathway.

ABSTRACT:

Background

The restraint water immersion stress (RWIS) model includes both psychological and physical stimulation, which may lead to gastrointestinal disorders and cause gastric mucosal damage. The ventrolateral periaqueductal gray (VLPAG) contributes to gastrointestinal function, but whether it is involved in RWIS-induced gastric mucosal damage has not yet been reported.

Methods

The expression of glial fibrillary acidic protein (GFAP), neuronal c-Fos and phosphorylated extracellular signal regulated kinase 1/2 (p-ERK1/2) in the VLPAG after RWIS was assessed using western blotting and immunocytochemical staining methods. Lateral ventricle injection of astrocytic toxin L-a-aminoadipate (L-AA) and treatment with ERK1/2 signaling pathway inhibitor PD98059 were further used to study protein expression and distribution in the VLPAG after RWIS.

Results

The expression of c-Fos, GFAP, and p-ERK1/2 in the VLPAG significantly increased following RWIS and peaked at 1 h after RWIS. Lateral ventricle injection of the astrocytic toxin L-AA significantly alleviated gastric mucosal injury and decreased the activation of neurons and astrocytes. Treatment with the ERK1/2 signaling pathway inhibitor PD98059 obviously suppressed gastric mucosal damage as well as the RWIS-induced activation of neurons and astrocytes in the VLPAG.

Conclusions

These results suggested that activation of VLPAG neurons and astrocytes induced by RWIS through the ERK1/2 signaling pathway may play a critical role in RWIS-induced gastric mucosa damage.

SUBMITTER: Gao W

PROVIDER: S-EPMC8378083 | biostudies-literature |

REPOSITORIES: biostudies-literature

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