Neural and hormonal mechanisms Flashcards
Homeostasis
Homeostasis is the mechanism by which an organism maintains a steady internal environment. Part of homeostasis is detecting whether the body has enough nutrients and correcting the situation if this is not the case. The body has evolved to separate systems for achieving this, one for turning heating on and one for turning it off. For humans, glucose levels probably play the most important role in producing feelings of hunger. Hunger increases as glucose levels decrease. A decline in glucose levels in the blood activates a part of the brain called the lateral hypothalamus, resulting in feelings of hunger. This causes the individual to search for and consume food, which causes glucose levels to rise again.This rising glucose levels activates the ventral medial hypothalamus, which leads to feelings of citation, which intern inhibits further feeding. In some animals, however, this does not happen, as can be seen from studies of the protein leptin.
Lateral hypothalamus
Researchers discovered in the 1950s that damaged to the lateral hypothalamus in rats caused a condition called aphagia (absence of eating). Research is also found that the stimulation of the lateral hypothalamus illicit feeding behaviour. These opposing effects of injury and stimulation lead researchers to conclude that they had discovered the OnSwitch for eating behaviour. A neurotransmitter found in the hypothalamus called neuropeptide Y is particularly important in turning on eating.When injected into the lateral hypothalamus of rats, neuropeptide Y causes them to immediately begin feeding, even when satted (Reynolds and Wickens). Repeated injections of NPY into the hypothalamus of rats producers obesity in just a few days (Stanley).
Ventromedial hypothalamus
In contrast to the effective damage to the lateral hypothalamus, research is also discovered that damage to the ventory medial hypothalamus causes wraps to ovary, leading to a condition called hyperphagia. Similarly, stimulation of this area inhibited feeding. This lead research is to conclude that the VMH signals stop eating as a result of the many glucose receptors in this area. However, damage to the nerve fibre is passing through the VMH tends to also damage another area of the hypothalamus, the paraventricular nucleus, and is now believed that damage to the PV and alone causes hyperphagia (gold). The PVN also detects the specific foods our body needs, and consequently seems to be responsible for many of our cravings.
Ghrelin
Released in the stomach and sometimes the hypothalamus, to increase appetite. If a persons body resources allow or if they are undereating, then ghrelin levels increase. Ghrelin levels also have a role in determining how quickly we feel hungry again after we’ve eaten. They go up dramatically before we eat and then go down again for about three hours after a meal. Ghrelin is thought to be important in the development of obesity because, and stimulating appetite, it leads to an increase inbody weight. Ghrelins role in appetite control was first noted when it was discovered that when grilling was injected into the bloodstream of rats, it stimulated food intake. Other evidence came from the observation that my slacking either ghrelin or its receptor in the hypothalamus are protected fromdiet induced obesity.
Leptin
In 1994, researchers noticed that when they administered a new substance to genetically altered obese laboratory mice, the mice lost weight. Leptin, as this new substance became known, is a hormone that plays a crucial role in appetite and weight control. It is normally produced by fat tissue and secreted into the bloodstream, where it travels to the brain and decreases appetite. Circulating leptin levels act as a long-term signal of the amount of fats stored in adipose tissue, whilst short-term fluctuations in leptin levels provide information regarding changes in calorific intake. Leptin is thought to have two major of functions. By binding into receptions in the hypothalamus, it counteracts the effects of NPY, a feeding stimulant secreted in the bloodstream and the hypothalamus. Secondly, leptin increases sympathetic nervous system activity, which stimulates fatty tissue burn energy.
Evaluation – limitations of a homeostatic explanation
For hunger mechanism to be adaptive, it must both anticipate and prevent energy deficits, not just react to them. As a result, the theory that hunger and eating is triggered only when energy resources fall below their desired level is incompatible with the heart reality in which such systems would’ve evolved. Such a mechanism to be truly adaptive, it must promote levels of consumption that maintain delivery resources well above the optimal level to act as a buffer against future lack of food availability. Explanations of food intake based solely on homeostatic mechanisms of a limited perspective on eating behaviour.
Problems with the role of the lateral hypothalamus
The view that the lateral hypothalamus served as an on switch for eating turned out to have a few problems. For example, that damage to the lateral hypothalamus caused deficits in other aspects of behaviour, for example, thirst and sex, rather than just hunger. Also, more recent research has shown that each behaviour is controlled by neural circuits that run throughout the brain, and not just by the hypothalamus. Although the lateral hypothalamus undoubtedly plays an important role in controlling eating behaviour, it is not, as previously thought, the brains eating centre(Sakurai).
Support for the role of the ventromedial hypothalamus
Early research has found that lesions or damage to the VMH resulted in hyperphasia and obesity in a number of different species, including humans. This led them to designate the VMH as the society centre in eating behaviour, with the PVN having a particularly important role in the process (Gold). Most studies showed that, compared to lesions in other brain areas, animals with VMH lesions are substantially more and gained substantially more weight, supporting the important role role played by this region in the control of eating.
