Gastric electrical stimulation improves enteric neuronal survival

Area of Science:

• Gastroenterology
• Neuroscience
• Cell Biology

Background:

• Vagotomy, a surgical procedure affecting the vagus nerve, significantly impacts gastrointestinal motility.
• Damage to the central nervous system, including the vagus nerve, can lead to severe physiological dysfunction in the gut.
• Enteric neurons are crucial for regulating gastrointestinal function, and their survival is vital for gut health.

Purpose of the Study:

• To investigate the effects of synchronized dual-pulse gastric electrical stimulation (SGES) on enteric neuron apoptosis in vagotomized rats.
• To explore the potential molecular pathways, including connexin 43 (Cx43), glial cell line-derived neurotrophic factor (GDNF), and the PI3K/Akt pathway, involved in SGES-mediated neuroprotection.
• To assess the impact of short-term and long-term SGES on neuronal survival and apoptosis markers following subdiaphragmatic vagotomy.

Main Methods:

• Male Sprague-Dawley rats underwent subdiaphragmatic vagotomy and were divided into control, vagotomy-only, and vagotomy with short-term or long-term SGES groups.
• Expression levels of Cx43, GDNF, p-Akt, pan-Akt, and PGP9.5 were quantified using RT-qPCR, Western blot, and immunofluorescence.
• Apoptosis was evaluated using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay.

Main Results:

• Vagotomy led to decreased expression of Cx43, GDNF, and PGP9.5, and increased neuronal apoptosis (TUNEL-positive cells).
• SGES treatment significantly upregulated Cx43, GDNF, and PGP9.5 expression in vagotomized rats.
• SGES reduced the number of TUNEL-positive cells, indicating decreased apoptosis, and increased p-Akt expression, suggesting PI3K/Akt pathway activation.

Conclusions:

• Synchronized dual-pulse gastric electrical stimulation (SGES) demonstrates a protective effect on enteric neurons against vagotomy-induced apoptosis.
• SGES may exert its neuroprotective effects by upregulating Cx43 and GDNF expression.
• The phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway appears to be involved in the mechanism by which SGES promotes enteric neuronal survival.