Altered Neuronal Activity in the Central Nucleus of the Amygdala Induced by Restraint Water-Immersion Stress in Rats

Feng He,Xiusong Wang,Xiwen Geng,Min Wang,Hongbin Ai

doi:10.1007/s12264-018-0282-y

Abstract

Restraint water-immersion stress (RWIS), a compound stress model, has been widely used to induce acute gastric ulceration in rats. A wealth of evidence suggests that the central nucleus of the amygdala (CEA) is a focal region for mediating the biological response to stress. Different stressors induce distinct alterations of neuronal activity in the CEA; however, few studies have reported the characteristics of CEA neuronal activity induced by RWIS. Therefore, we explored this issue using immunohistochemistry and in vivo extracellular single-unit recording. Our results showed that RWIS and restraint stress (RS) differentially changed the c-Fos expression and firing properties of neurons in the medial CEA. In addition, RWIS, but not RS, induced the activation of corticotropin-releasing hormone neurons in the CEA. These findings suggested that specific neuronal activation in the CEA is involved in the formation of RWIS-induced gastric ulcers. This study also provides a possible theoretical explanation for the different gastric dysfunctions induced by different stressors.

Highlights

Restraint water-immersion stress (RWIS) is widely accepted as a useful procedure to induce gastric ulceration in rats [1,2,3]
A–B Two representative examples of coronal sections stained with neutral red, photographed at low magnification, demonstrating the positions of microelectrode tips in the medial part of the central nucleus of the amygdala and the lateral part of the central nucleus of the amygdala
As the main output of the amygdala, the central nucleus of the amygdala (CEA) is differentially activated by various stressors and deeply involved in autonomic regulation as well as stress-related behaviors [14, 30,31,32]

Summary

Introduction

Restraint water-immersion stress (RWIS) is widely accepted as a useful procedure to induce gastric ulceration in rats [1,2,3]. Physiological studies have demonstrated that electrical stimulation of different regions of the CEA induces increased gastric acid secretion [10], increased or decreased gastric motility [11, 12], gastric ulceration [13], and altered activity of neurons in the NST and DMV [9, 12] Together, both anatomical and physiological studies suggest that the CEA plays an important role in the mechanisms underlying the formation of stress-induced ulcers. As demonstrated previously [14,15,16,17], stressors such as immobilization, starvation, pain, hypoglycemia, and foot shock induce c-Fos expression at different levels in the CEA, but stressors such as cold and blood-loss do not It is unclear whether RWIS changes neuronal activity in the CEA

Methods

Results

Conclusion