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{{Image|Lachapskull.jpg|right|220px|Homo neanderthalensis skull from La Chapelle-aux-Saints, France.}}
'''[[Gut-brain signalling]]''' describes the interaction between the gastrointestinal tract and the brain, and how secretion of varying hormones from different areas of the body causes appetite-enhancing and satiety signals to be sent to the brain. The hormones that have been most intensely studied are: ghrelin, obestatin, cholecystokinin (CCK), GLP-1, peptide YY (PYY) and insulin which all play major roles in appetite regulation.  The vagus nerve is also a key mediator of regulation, and all of these inputs are processed by areas in the brain such as the hypothalamus and the nucleus tractus solitarii (NTS).
The '''[[Neanderthal]]s''' are an extinct nonmodern hominid that come chronologically extremely close to the modern era, becoming extinct less than 30,000 years ago. The classic Neanderthal traits are found from about 75,000 to 35,000 years ago, but it is difficult to date the initial appearance of this species. Without great dating techniques, the best early estimate comes from the Moula Guercy site in France dating the earliest appearance of Neanderthals to 120,000 years ago.


For decades the Neanderthals have been viewed as a hunched, hairy, stumbling, stupid cave man that lived tens of thousands of years ago. This image can be highly attributed to Marcellin Boule, a French paleoanthropologist at the beginning of the twentieth century. In 1908, at La Chapelle-aux-Saints in southwestern France a nearly complete male skeleton was excavated and Boule spent the better part of three years examining this specimen. The man was old in terms of Neanderthal standards, aging between 40 and 50 years old and suffered from severe arthritis in his spine. This fact was discovered long after Boule described him as hunched over, practicing an inefficient shuffling gait type of bipedalism. His preconceptions, opposed to scientific objectivity, resulted in the misconception about the genus as a whole. Today this is reflected in not only in normal perception but shown in popular culture, specifically the insurance company that concludes their process is "So Easy, a Caveman Can Do It." Interestingly, these commercials counter react the misconceptions by having offended cavemen be present and engaged in modern, human-like behavior, highlighting the misconception placed by Boule a hundred years ago.
==Anorexic Signals==
{{Image|diagram 3.jpg|right|400px|''Gut-Brain signaling Pathways'' Proteins and hormones activate brain pathways in different ways, either by eventual vagal activation or through peripheral circulation. The nucleus tractus solitarii and the arcuate nucleus are then activated. }}
'''Cholecystokinin''' (CCK) is a peptide hormone synthesised  by L-cells in the mucosal epithelium of the duodenum, and secreted in response to the presence of partly digested lipids and protein]]s. CCK inhibits gastric emptying and stimulates the release of digestive enzymes from the pancreas and bile from the gall bladder by acting at CCK-A receptors (mainly found in the periphery but also found in some areas of the CNS). Because gastric emptying is inhibited, the partly digested lipids and proteins are exposed to the digestive enzymes and bile so are further broken down. As the lipids and proteins are broken down, CCK secretion declines.  


===Discovery===
CCK acts as a ‘gatekeeper’ for the response of other gut-brain signalling hormones on the afferent vagal neurons. At low levels (after fasting), CCK stimulates the expression of receptors associated with the stimulation of food intake, including receptors for melanin concentrating hormone (MCH)-1 and cannabinoid CB1 receptors. At high levels (after food consumption), MCH-1 and CB1 receptors are down- regulated. Therefore CCK, at a high or low concentration, can affect how afferent vagal neurons respond to other neurohormones.
Neander Valley, literally translated in German as "Neandertal", in the German Federal State of North Rhine-Westphalia, where the river Düssel flows to meet the Rhine. It is here that the first fossil to be recognized as a different kind of human was discovered. It this day in August of 1856 that many claim to be beginning of the field of paleoanthropology. Miners in search of limestone blasted open the entrance to a small cave, Feldhofer Cave (also called Feldhofer Grotto) where an array of fossilized bones were found. The miners mostly discarded the bones, but sat some aside to bring to a local school teacher, believing them to be bones from a cave bear. Included in this group was the skullcap that will eventually become the holotype of Homo neanderthalensis. The fossil displays a long skull joining with very pronounced brow ridges above the orbits. In addition, the miners came across two femora, five arm bones, part of the left ilium, portions of a scapula and multiple ribs. These fossils were delivered to a school teacher and amateur natural historian, Johann Fuhlrott.


[[Neanderthal|....]]
In rats, CCK inhibits food intake in younger individuals more effectively than in older individuals. It also has a greater effect in males than in females.
 
'''Glucagon-like peptide-1''' (GLP-1) is a hormone secreted from L-cells in the mucosal epithelium of the duodenum and small intestine. It is derived from the ''pro-glucagon'' gene, and is secreted into the circulation in response to the presence of nutrients. It acts at the pancreas, where it stimulates insulin secretion and suppresses glucagon secretion. It also increases insulin sensitivity. GLP-1 also activates anorexigenic neurons in the arcuate nucleus via the caudal brainstem. Activation of these  neurons induces satiety and decreases food intake/hunger. It also decreases gastric emptying, so adds to the feeling of being ‘full’. At higher concentrations, GLP-1 causes nausea, and can induce conditioned taste aversion, where the brain associates the taste of a certain food with being toxic (usually after an individual consumes a food that had made them sick).
 
[[Gut-brain signalling|.....]]

Revision as of 23:54, 22 July 2011

Gut-brain signalling describes the interaction between the gastrointestinal tract and the brain, and how secretion of varying hormones from different areas of the body causes appetite-enhancing and satiety signals to be sent to the brain. The hormones that have been most intensely studied are: ghrelin, obestatin, cholecystokinin (CCK), GLP-1, peptide YY (PYY) and insulin which all play major roles in appetite regulation. The vagus nerve is also a key mediator of regulation, and all of these inputs are processed by areas in the brain such as the hypothalamus and the nucleus tractus solitarii (NTS).

Anorexic Signals

Gut-Brain signaling Pathways Proteins and hormones activate brain pathways in different ways, either by eventual vagal activation or through peripheral circulation. The nucleus tractus solitarii and the arcuate nucleus are then activated.

Cholecystokinin (CCK) is a peptide hormone synthesised by L-cells in the mucosal epithelium of the duodenum, and secreted in response to the presence of partly digested lipids and protein]]s. CCK inhibits gastric emptying and stimulates the release of digestive enzymes from the pancreas and bile from the gall bladder by acting at CCK-A receptors (mainly found in the periphery but also found in some areas of the CNS). Because gastric emptying is inhibited, the partly digested lipids and proteins are exposed to the digestive enzymes and bile so are further broken down. As the lipids and proteins are broken down, CCK secretion declines.

CCK acts as a ‘gatekeeper’ for the response of other gut-brain signalling hormones on the afferent vagal neurons. At low levels (after fasting), CCK stimulates the expression of receptors associated with the stimulation of food intake, including receptors for melanin concentrating hormone (MCH)-1 and cannabinoid CB1 receptors. At high levels (after food consumption), MCH-1 and CB1 receptors are down- regulated. Therefore CCK, at a high or low concentration, can affect how afferent vagal neurons respond to other neurohormones.

In rats, CCK inhibits food intake in younger individuals more effectively than in older individuals. It also has a greater effect in males than in females.

Glucagon-like peptide-1 (GLP-1) is a hormone secreted from L-cells in the mucosal epithelium of the duodenum and small intestine. It is derived from the pro-glucagon gene, and is secreted into the circulation in response to the presence of nutrients. It acts at the pancreas, where it stimulates insulin secretion and suppresses glucagon secretion. It also increases insulin sensitivity. GLP-1 also activates anorexigenic neurons in the arcuate nucleus via the caudal brainstem. Activation of these neurons induces satiety and decreases food intake/hunger. It also decreases gastric emptying, so adds to the feeling of being ‘full’. At higher concentrations, GLP-1 causes nausea, and can induce conditioned taste aversion, where the brain associates the taste of a certain food with being toxic (usually after an individual consumes a food that had made them sick).

.....

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