Central Nervous System Control of Gastrointestinal Motility and Secretion and Modulation of Gastrointestinal Functions

Abstract

Although the gastrointestinal (GI) tract possesses intrinsic neural plexuses that allow a significant degree of autonomy over GI functions, the central nervous system (CNS) provides extrinsic neural inputs that regulate, modulate, and control these functions. While the intestines are capable of functioning in the absence of extrinsic inputs, the stomach and esophagus are much more dependent upon extrinsic neural inputs, particularly from parasympathetic and sympathetic pathways. The sympathetic nervous system exerts a predominantly inhibitory effect upon GI muscle and provides a tonic inhibitory influence over mucosal secretion while, at the same time, regulates GI blood flow via neurally mediated vasoconstriction. The parasympathetic nervous system, in contrast, exerts both excitatory and inhibitory control over gastric and intestinal tone and motility. Although GI functions are controlled by the autonomic nervous system and occur, by and large, independently of conscious perception, it is clear that the higher CNS centers influence homeostatic control as well as cognitive and behavioral functions. This review will describe the basic neural circuitry of extrinsic inputs to the GI tract as well as the major CNS nuclei that innervate and modulate the activity of these pathways. The role of CNS-centered reflexes in the regulation of GI functions will be discussed as will modulation of these reflexes under both physiological and pathophysiological conditions. Finally, future directions within the field will be discussed in terms of important questions that remain to be resolved and advances in technology that may help provide these answers.

White Matter Microstructural Similarity and Diversity of Functional Constipation and Constipation-predominant Irritable Bowel Syndrome

“…A previous study showed that preganglionic motor neurons provide vagal innervations to the gastrointestinal tract and stem from the dorsal motor nucleus of the vagus nerve within the brainstem. 12 Moreover, Lim et al reported that the colon transit time was delayed in patients with pontine lesions (a part of the brainstem). 58 Therefore, we suspected that the aberrations in the CR associated with the corticopontine tract may be linked with CNS dysregulation of colon transit time in constipated patients.…”

“…However, the data supporting different etiologies between FC and IBS-C are scant. A significant number of published studies have attributed the symptoms of functional gastrointestinal disorders (FGIDs) to dysregulation of the brain-gut axis (BGA) [10][11][12][13][14][15][16] that reflects a framework account for bidirectional interactions between the central nervous system (CNS), autonomic nervous system (ANS), and enteric nervous system (ENS). Within the framework, the CNS integrates communication within the BGA, thereby enabling the CNS to regulate the ENS via sympathetic and parasympathetic pathways.…”

“…Within the framework, the CNS integrates communication within the BGA, thereby enabling the CNS to regulate the ENS via sympathetic and parasympathetic pathways. 12 The ENS in turn works through local excitatory and inhibitory motor neurons that release neurotransmitters. 11 As 2 types of FGIDs, FC, and IBS-C have also been demonstrated to be associated with BGA disorders, in which the brain neural system was reported to have momentous functions.…”

“…11 As 2 types of FGIDs, FC, and IBS-C have also been demonstrated to be associated with BGA disorders, in which the brain neural system was reported to have momentous functions. [10][11][12][13] Therefore, CNS studies could make it easier to understand the differentiation between FC and IBS-C. Recently, the rapid advancement of neuroimaging techniques made it convenient to investigate CNS mechanisms underlying various diseases including IBS and FC.…”

Vagus nerve stimulation mediates protection from kidney ischemia-reperfusion injury through α7nAChR+ splenocytes

“…Vagovagal reflexes are well described in gastrointestinal physiology (40). Vagal afferents activated by inflammation are believed to trigger a vagovagal reflex that elicits the CAP (41,42).…”