Neural Control of the Gastrointestinal System

Introduction

Motility and secretion are controlled through neural, hormonal, and paracrine systems. The hierarchy of neural control begins in the enteric nervous system (ENS), a localized intrinsic system able to self-regulate control. Modification and regulation of gastrointestinal (GI) function also occurs with help of higher brain centers within the central nervous system (CNS), and the autonomic nervous system (ANS), which is comprised of sympathetic and parasympathetic branches. The sympathetic nervous system predominantly provides inhibitory feedback slowing gastric motility, decreasing mucosal secretion, and diverting blood supply away from GI tract. The parasympathetic nervous system largely functions as the opposite of the sympathetic nervous system and generally stimulates the GI tract. Neural centers are regulated by one another through sensory feedback pathways, which travel in autonomic nerves. The full circuit creates feedback loops forming reflexes regulated by the CNS or ENS. Gastric function is often presumed to be an unconscious process but higher brain centers in the CNS are influenced by emotion and cognition and can alter function. This chapter will focus on the anatomy, and physiology associated with the neural pathways, which control the GI system.

Central Nervous System Control

Although gastric function is able to operate through enteric mechanisms, extrinsic input from the CNS is essential to maintain organized digestion. Higher command centers in the brain initiate vagal efferent, descending pathways in the spinal cord, which connect to preganglionic neurons in the thoracolumbar and sacral regions. Studies using retrograde transneuronal viruses have identified GI neurological involvement in the nucleus tractus solitaries (NTS), parabrachial complex, hypothalamus, amygdala, area postrema, and periaquadectal gray matter ( ). These locations alter efferent signals by receiving sensory information originating from parasympathetic, and sympathetic afferents from the viscera. The conglomeration of sensory information from throughout the GI tract helps modify outflow signals to particular regions.

The NTS acts as the only CNS input center for both parasympathetic and sympathetic sensory information. Spinal sensory input within the NTS facilitates communication with other CNS nuclei, altering control of efferent signaling to the GI tract ( ). Visceral afferent signals are relayed to the CNS via parasympathetic vagal afferents while nociceptive stimulation from the GI system are relayed by sympathetic, spinal, afferent signals. The visceral afferents are thought to carry physiologic information like distention, motility, satiety, and nausea. The convergence of sympathetic and parasympathetic afferents to the NTS facilitates efferent information, influencing output from both ANSs ( ).

Mechanisms of signaling from specific CNS centers to other centers is largely unknown. As some CNS centers in the brainstem remain outside of the blood-brain barrier, it is proposed that accessibility to various hormones, cytokines, and neuromodulators plays a role in GI modulation ( ). Regions such as the frontal cerebral cortex, stria terminalis, parabrachial complex, hypothalamus, amygdala, and periaqueductal gray matter have projections to vagal output centers in the medulla oblongata ( ). These regions have pathways within the limbic region of the brain, which is known to process emotional responses. These connections may explain how cognitive changes such as stress, change in sleep patterns, depression, and emotional events may induce GI symptoms such as nausea, diarrhea, decreased food intake, abdominal pain, and emesis ( ).

The understanding of how CNS pathways maintain homeostasis within the GI tract is incompletely understood. Further understanding requires analysis of neurological and hormonal changes that are related to physiological phenomena within the GI system. The association of cognition and emotion with functional GI disorders provides opportunity for novel therapeutic interventions.