Digestive and nervous system relationship

How do the brain and digestive system work together? | Digestive Health - Sharecare

digestive and nervous system relationship

The nervous system exerts a profound influence on all digestive processes, namely Connection to the central nervous system also means that signals from . It is helpful to understand the similarities and connections between the brain and the digestive system. The gut is controlled by the enteric nervous. The brain controls the contraction of skeletal muscle. The nervous system regulates the speed at which food moves through the digestive tract.

Lungs, larynx, pharynx, trachea, bronchi The brain monitors respiratory volume and blood gas levels. The brain regulates respiratory rate.

Digestive System The digestive system stores and digests foods, transfers nutrients to the body, eliminates waste and absorbs water.

digestive and nervous system relationship

Stomach, esophagus, salivary glands, liver, gallbladder, pancreas, intestines Digestive processes provide the building blocks for some neurotransmitters.

The autonomic nervous system controls the tone of the digestive tract. The brain controls drinking and feeding behavior. The brain controls muscles for eating and elimination. The digestive system sends sensory information to the brain. Reproductive System The reproductive system is responsible for producing new life.

digestive and nervous system relationship

Testes, vas deferens, prostate gland, ovary, fallopian tubes, uterus, cervix Reproductive hormones affect brain development and sexual behavior. The brain controls mating behavior. Urinary System The urinary system eliminates waste products and maintains water balance and chemical balance. Bladder, urethra, kidney The bladder sends sensory information to the brain. Curious about whether isolating and stimulating individual components of the complex array of signals converging in the NTS would reflect what normally occurs during a meal, Moran and colleagues compared c-fos activation in a real versus a sham feeding 4 situation Emond et al.

They observed a much greater degree of activation in the taste region of the NTS in the sham feeding situation, suggesting that the brain processes and responds to oral signals differently depending on where in the GI tract nutrients are present.

Other kinds of alterations e. Only recently have scientists discovered taste-like cells in the gut as well. Robert Margolskee provided an overview of taste receptors in the oral cavity and discussed recent research on taste-like receptors in the gut.

Taste Receptors in the Oral Cavity Oral taste buds—collections of about 50 to specialized epithelial cells—are scattered throughout the oral cavity, primarily in papillae 6 on the front, sides, and back of the tongue. Although oral taste buds are not neurons, they have a number of neuronal properties. Much of the taste transduction cellular machinery is contained within the fingerlike microvilli coating the apical end of each taste bud cell.

Margolskee explained that scientists have identified several different types of taste receptors in the oral cavity, each having a unique taste receptor molecule or set of molecules underlying the taste response Lindemann, Over the past decade, work from Margolskee's laboratory, as well as the laboratories of Linda Buck, Nick Ryba, and Charles Zucker, has led to identification of many of the different taste quality receptors.

Today, researchers know that the bitter taste receptors involve a family of about 25 to 30 G protein-coupled receptors 7 called the T2Rs type 2 taste receptors. Sweet receptors, in contrast, involve a dimeric or multimeric combination of T1R2 type 1 receptor 2 and T1R3 type 1 receptor 3 receptors, which together respond to a number of sweet compounds, both sugars and noncaloric sweeteners. The sour and salty taste transduction channels are not as well understood as the bitter, sweet, and umami channels, said Margolskee.

Although ENaC 8 certainly plays a role in salty taste transduction, it is involved more with low concentrations of salt.

There is likely at least one other transduction channel, as yet unidentified, for high concentrations of salt.

The sour taste receptor has a number of candidate channels, including acid-sensing ion channels ASICshyperpolarization-activated cyclic nucleotide-gated HCN channels, and polycystic kidney disease PKD family member channels, but no one channel has yet been definitively identified.

Nerves and the Digestive System

Taste-Like Cells in the Gut and Pancreas As summarized by Margolskee, researchers recently have identified taste-like cells in the gut that play an important role in integrating physiological responses during digestion. Taste-like cells in the gut are not actual taste cells, although they have a number of characteristics in common with true oral taste cells: Indeed, the signaling process that occurs in certain types of endocrine cells in the gut is very similar to the transduction process that occurs in oral taste cells Cummings and Overduin, see Figure In both types of cells, when G protein-coupled receptors at the apical surface of the cell couple with gustducin and other taste-associated G proteins, they initiate a signal transduction cascade involving multiple signaling enzymes, second messengers e.

Margolskee explained that one of the differences between taste receptors in the oral cavity and taste-like receptors in the gut is that instead of releasing a true neurotransmitter, taste-like receptors in the gut release neuropeptide hormones, such as GLP-1 glucagon-like peptide Modified from Cummings and Overduin, Reprinted with permission of the American Society for Clincial more Subsequently, Enrique Rozengurt's group identified a number of T2R bitter taste receptors in the stomach and small intestine Wu et al.

In more detailed microscopic studies, Shirazi-Beechey and Margolskee collaborated and found that both T1R2 and T1R3, the two components of the sweet receptor, are present in a small subset of cells lining the small intestinal mucosa and that the cells have the typical appearance of enteroendocrine cells Margolskee et al. Margolskee and his team also collaborated with Josephine Egan at the National Institutes of Health and identified several taste signaling proteins in both human and mouse tissues.

digestive and nervous system relationship

They also found essentially the entire taste transduction pathway as it was known to exist in oral taste cells, in gut endocrine cells, and particularly in L cells expressing GLP-1 Jang et al. Li also found a number of short chain fatty acids co-expressed with alpha-gustducin in endocrine cells in the colon, including cells activated by the G protein-coupled receptors GPR43 and GPR Curious about the potential physiological role of gustducin in the colon, she turned to gustducin knockout mice and found that short chain fatty acid—stimulated GLP-1 secretion from colon endocrine cells requires alpha-gustducin.

Enteric Nervous System

In other collaborative work between Margolskee's laboratory and Shirazi-Beechey's group, the researchers examined SGLT1 sodium glucose co-transporter 1 expression in two types of knockout mice Margolskee et al. SGLT1 is a protein that co-transports glucose and sodium from the gut lumen across the absorptive enterocytes and into the epithelial cells.

According to Margolskee, this is typically the rate-limiting step for glucose uptake in the small intestine. But in knockout mice missing T1R3, a component of both the sweet and umami receptors, there was no difference in SGLT1 between the low- and high-carbohydrate diets. Likewise with gustducin knockout mice, the research revealed no difference in SGLT1 mRNA or protein or glucose uptake activity between the low- and high-carbohydrate diets.

According to Margolskee, the evidence suggests that both T1R3 and gustducin are necessary to elicit an increase in SGLT1 in response to dietary carbohydrate and a subsequent increase in glucose uptake activity. Margolskee described a similar effect observed in knockout mice fed either a low-carbohydrate diet alone or a low-carbohydrate diet supplemented with a noncaloric sweetener i.

These results indicate a chemosensory detection pathway in the gut that responds to luminal sugars and luminal sweeteners and leads to the up-regulation of SGLT1 and an increase in glucose uptake activity across the gut. Margolskee and others have found taste-like receptors not just in the stomach and intestine but also in the pancreas.

digestive and nervous system relationship

Margolskee described unpublished data showing the expression of gustducin in pancreatic islet alpha cells and the expression of T1R3 in both alpha and beta cells. The function of these pancreas taste-like receptors is unclear. However, both in vitro data and data from wild-type versus T1R3 knockout mice suggest that these receptors play a role in sweetener-enhanced insulin release.

Oral taste cells also express intestinal sugar sensors, such as SGLT1, and pancreatic metabolic sensors Yee et al. Margolskee gave an example of the expression of gut proteins in the oral cavity.

Based on studies with T1R3 knockout mice showing a loss of response to noncaloric sweeteners but not to sugars Damak et al. They hypothesized the presence of a glucose transport pathway similar to what has been observed in pancreatic beta cells. Indeed, they found that a number of the same pancreatic pathway components were present in oral taste tissue Yee et al.

Margolskee speculated that gut-like glucose transporters in taste cells may help people and animals distinguish caloric from noncaloric sweeteners. Taste-Like Receptors in the Gut and Pancreas: Summary of the Science In summary, Margolskee noted that researchers have identified whole taste signaling pathways in both the gut and pancreas and in both the proximal and distal gut.

In the pancreas, both pancreatic islet alpha and beta cells express taste elements. In the colon, gustducin appears to be involved in the release of GLP-1 and GIP in response to short-chain fatty acids. With regard to the role of taste signaling molecules in the pancreas, preliminary evidence suggests that gustducin and T1R3 are involved in sweetener detection and, under some circumstances, insulin secretion. He focused on CCK because scientists know more about how it modulates vagal afferent activity compared with what is known about other GI peptides.

GI Peptides GI peptides are localized in specialized enteroendocrine cells scattered among the cells of the absorptive and secretory mucosa of the GI tract, from the stomach through the colon.

Nerve fibers pass through the extracellular space beneath the mucosa, into which GI peptide secretion occurs, creating the opportunity for both endocrine and neuronal peptide actions.

How do the brain and digestive system work together?

According to Ritter, although the actions of some GI peptides were discovered in the early 20th century e. A dozen or more GI peptides have been identified to date. Several are involved in control of food intake, including CCK, which is secreted in the proximal small intestine, and GLP-1, PYY peptide tyrosine tyrosineand oxyntomodulin, all of which are secreted by L cells in the more distal small intestine and large intestine.

Ghrelin, which is released from cells in the gastric mucosa, increases food intake. Ritter went on to explain that after their secretion from enteroendocrine cells, GI peptides in the blood can broadcast a signal to any tissue with a matching receptor, including tissues in GI organs where the peptides help coordinate digestive function.

Early during the digestive process, they contribute to slowing gastric emptying and stimulating pancreatic secretion of enzymes and bicarbonate. Later they facilitate secretion of insulin and the postabsorptive assimilation of nutrients see the review by Rehfeld, GI peptides also play an important role in limiting food intake.

In Ritter's opinion, food intake can be viewed as yet another part of the digestive process, given that reducing food intake limits the inflow of food into the digestive tract during a meal and thereby facilitates the efficient digestion and absorption of what has been eaten. In addition to their impact on GI tissues, GI peptides act on the brain and innervation of the GI tract see reviews by Banks, ; de Lartigue, ; and Schwartz, According to Ritter, a hallmark of GI peptides is that their secretion and levels in circulation are controlled by nutrients in the GI tract during a meal.

When a meal is eaten, levels of GI peptides in the blood rise dramatically Ellrichmann et al. Initially, upon entry of nutrients into the intestine, CCK levels rise rapidly to six or seven times their fasting level. The initial rapid rise in CCK levels has been shown to facilitate the release of the other peptides in anticipation of actual direct stimulation of their secretion by nutrients as food moves down through the intestine.

Another hallmark of GI peptides, according to Ritter, is that their impact on the control of food intake is focused on limiting the size and duration of an ingested meal. CCK, GLP-1, and PYY all reduce food intake, primarily by reducing meal size and meal duration rather than by decreasing the number of meals initiated see the review by Ritter, According to Ritter, a vagal mode of action characterizes not only CCK but most other GI peptides as well; in fact, their ability to reduce food intake is attenuated or virtually abolished when the abdominal vagus nerve is cut.

For ghrelin, however, the stimulatory effect on food intake is more complicated. According to Ritter, ghrelin appears to antagonize the excitatory effects of some of the other GI peptides on vagal afferent firing, although a role for the vagus in actually mediating the increase in food intake through ghrelin is doubtful. All vagal afferents release glutamate, a neurotransmitter, in the hindbrain. Thus, not surprisingly in Ritter's opinion, CCK-induced reduction of food intake has been shown to be sensitive to antagonism of glutamate receptors in the hindbrain.

In fact, antagonism of NMDA-type N-methyl-D-aspartate glutamate receptors with selective receptor antagonists injected directly into the hindbrain reverses or prevents reduction of food intake by exogenously administered CCK Wright et al. An interesting feature of vagal afferent fibers, according to Ritter, is their very quick release of all available neurotransmitters and failure over time. Susan Appleyard has shown that upon stimulation of vagal afferent inputs, postsynaptic cells fire but then fail; however, their failure can be reversed by local application of CCK Appleyard et al.

In terms of the specific cellular mechanism by which CCK enhances vagal afferent transmission, Ritter has found that CCK activates an enzyme, an extracellular receptor kinase, that phosphorylates synapsin. Synapsins are proteins that bind synaptic vesicles to the cytoskeleton of the neuron; they help control the availability of neurotransmitters for release. When phosphorylated, synaptic vesicles are freed from the cytoskeleton and the availability of transmitters for release is increased.

When dephosphorylated, the vesicles remain bound to the cytoskeleton of the neuron and fewer transmitters are available for release Cesca et al. Normally, CCK reduces food intake for only a short period of time, about 30 minutes, but inhibiting dephosphorylation of synapsin can extend and enhance the ability of CCK to reduce meal size Campos et al.

According to Ritter, it is not yet known whether other GI peptides operate in a similar way. The Impact of Non-GI Proteins on Food Intake Ritter emphasized that the GI signals controlling food intake are directly related to food that has just been consumed and is in the process of being digested and absorbed.

However, other parts of the physiology of an organism provide the brain with indirect information about metabolism that can also impact food intake. Some of this control emanates from connections between the digestive system and central nervous system, but just as importantly, the digestive system is endowed with its own, local nervous system referred to as the enteric or intrinsic nervous system.

The magnitude and complexity of the enteric nervous system is immense - it contains as many neurons as the spinal cord. The enteric nervous system, along with the sympathetic and parasympathetic nervous systems, constitute the autonomic nervous system.

The principal components of the enteric nervous system are two networks or plexuses of neurons, both of which are embedded in the wall of the digestive tract and extend from esophagus to anus: The myenteric plexus is located between the longitudinal and circular layers of muscle in the tunica muscularis and, appropriately, exerts control primarily over digestive tract motility.

digestive and nervous system relationship

The submucous plexus, as its name implies, is buried in the submucosa. Its principal role is in sensing the environment within the lumen, regulating gastrointestinal blood flow and controlling epithelial cell function.

In regions where these functions are minimal, such as the esophagus, the submucous plexus is sparse and may actually be missing in sections. The image below shows part of the myenteric plexus in a section of cat duodenum.

Pass your mouse cursor over the image to outline several enteric neurons. In addition to the two major enteric nerve plexuses, there are minor plexuses beneath the serosa, within the circular smooth muscle and in the mucosa.