Role of 5-HT1A receptor in insular cortex mediating stress – induced visceral sensory dysfunction

Abstract

Background

5-HT1A receptors (HTR1As) in the insular cortex are thought to be related with the generation of stress-induced functional gastrointestinal disorders (FGIDs), but its mechanism is not clear. Visceral hypersensitivity is one important pathophysiological mechanism of FGIDs. This study aimed to explore the role of HTR1As in mediating stress-induced visceral hypersensitivity and its mechanism in the insular cortex.

Methods

Visceral hypersensitivity rat model was established by water avoidance stress (WAS) and the visceral sensitivity was measured by electromyogram. The activities of HTR1As were regulated by microinjecting the HTR1A agonist and antagonist into the insular cortex. The expression levels of 5-HT, HTR1A, N-methyl-d-aspartic acid receptor subtype 2B (NR2B) and c-fos were observed by RT-PCR, Western Blot and immunohistochemical staining.

Key Results

In WAS rats, the expression levels of 5-HT and HTR1As in the insular cortex were significantly lower (p < 0.05) than that in sham WAS and normal rats, but the levels of c-fos and NR2B were significantly higher (p < 0.05). After microinjecting HTR1As agonist into the insular cortex of WAS rats, the visceral sensitivity and the expression levels of NR2B and c-fos in insular cortex significantly decreased (p < 0.05).

Conclusions & Inferences

The HTR1As-NR2B signal pathway of insular cortex plays an important role in regulating stress-induced visceral hypersensitivity.

This study aimed to explore the role of 5-HT1A receptors (HTR1As) in mediating stress-induced visceral hypersensitivity and its mechanism in the insular cortex. The results indicated that HTR1A in the insular cortex plays an important role in mediating chronic stress-induced visceral hypersensitivity in rats. N-methyl-d-aspartic acid receptor subtype 2B may be one of the important downstream signaling molecules of HTR1A mediating the visceral hypersensitivity.

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