The vagus nerve (cranial nerve X) originates in the brainstem, and extends through the neck, thorax, and abdomen, linking the brain to key organs of the gastrointestinal and cardiopulmonary systems. The motor division of the vagus nerve originates from two brainstem nuclei–the nucleus ambiguous (NAmb) and the dorsal motor nucleus of the vagus (DMV)–which modulate the motor and secretion control of the gastrointestinal (GI) tract. Sensory inputs from the GI tract are transmitted by vagal afferents to the nucleus tractus solitarius (NTS), which modulates DMV activity to coordinate processes like peristalsis, gastric secretion, and pancreatic functions. This complex network of motor and sensory pathways is vital for regulating GI function and maintaining homeostasis. Stress disrupts the excitatory-inhibitory balance within the DMV, leading to alterations in gastrointestinal motility and secretion. This imbalance plays a significant role in pathological conditions such as irritable bowel syndrome and functional dyspepsia. Furthermore, a crucial regulatory pathway from the substantia nigra pars compacta (SNpc) to the DMV modulates GI activity and is implicated in the etiology of Parkinson’s disease, where GI symptoms are often prodromal to motor dysfunction. In this context, vagal nerve stimulation emerges as a promising therapeutic approach, enhancing gut health and cognitive function through neuroprotection and inflammation reduction. These findings underscore the vital gut-brain connection in the treatment of neurological disorders.
Ozkaya et al. (2025) studied this question.