Abstract
Restraint water-immersion stress (RWIS), a compound stress model, includes both psychological and physical stimulation. Studies have shown that neurons in the hypothalamus are involved in RWIS, but the role of astrocytes and the interactions between astrocytes and neurons in RWIS are not clear. Here, we tested our hypothesis that hypothalamus astrocytes are involved in RWIS and interact with neurons to regulate gastric mucosal damage induced by RWIS. The expression of Glial fibrillary acidic protein (GFAP) and c-Fos in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) significantly increased following the RWIS. GFAP and c-Fos expression are similar in the temporal pattern, peaked at 1 h after the RWIS, then reduced gradually, and reached a maximal level again at 5 h which show “double-peak” characteristics. Intracerebroventricular administration of astroglial toxin L-a-aminoadipate (L-AA) and c-Fos antisense oligodeoxy nucleotides (ASO) both decreased RWIS-induced gastric mucosal damage. Results of immunohistochemistry assay revealed that both L-AA and ASO decreased the activation of astrocytes and neurons in the hypothalamus by RWIS. These results showed that hypothalamus neuron-astrocyte “network” involved in gastric mucosal damage induced by RWIS. This study may offer theoretical basis for some novel therapeutic strategies for RWIS-induced gastric ulcers.
Highlights
Restraint water-immersion stress (RWIS) in rats can imitate clinical gastric lesions caused by wounds, surgery or sepsis
The Glial fibrillary acidic protein (GFAP) expression in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) demonstrated a double-peak in which expression peaked at 1 h after administration of the RWIS reduced at 2 h and reached a maximal level again at 4–5 h (Figure 2G’)
We assessed hypothalamic astrocytes involved in RWIS-induced gastric mucosal damage in rats and examined interactions with hypothalamic neurons during this process
Summary
Restraint water-immersion stress (RWIS) in rats can imitate clinical gastric lesions caused by wounds, surgery or sepsis. RWIS is often used to study the etiopathogenesis of stress-induced gastric mucosal damage (Ai and Zhang, 1990; Ephgrave et al, 1997). Gastric function is primarily controlled by the parasympathetic nervous system through the dorsal motor nucleus of the vagus nerve (DMV; Andrews and Sanger, 2002; Hayakawa et al, 2003). Functional and anatomical connections among PVN neurons, the lower brainstem and spinal cord have been established. Parvocellular oxytocin (OT) cells in the PVN project mainly to the nucleus of solitary tract (NTS), the DMV and the intermediolateral cell column of the spinal cord
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