NEURAL MECHANISMS - created from Mind Map

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HOMEOSTASIS

mechanisms detect the state of the internal environment & act to restore the environment to its optimal state. there is a time lag between mechanisms operating to restore equilibrium & the body registering their effect. Even when the individual has eaten enough, only small amount is digested so only small amounts of nutrients are detected.

glucose controls hunger. low level = hungry, high level = satiety

IDA: for a hunger mechanism to be adaptive it must anticipate & prevent energy deficits, not just react to them. theory that hunger & eating are triggered only when energy sources fall below optimum, is incompatible with the harsh reality in which such systems would have evolved. to be truly adaptive it must promote levels of consumption that maintain bodily resources well above the optimal level for future lack of food. a better explanation would be evolutionary, where people eat because they develop a relish for particular tastes which in nature are associated with foods promoting survival.

such explanations may reductionist as they do not consider cognitive factors that also have a role in determining satiety. people are aware that they have just eaten & therefore logically assume they are full.

LATERAL & VENTROMEDIAL HYPOTHALAMUS

low glucose activates lateral hypothalamus, leading to feelings of hunger. Once food has been consumed as a results of this, glucose levels increase, activating ventromedial hypothalamus leading to satiation.

studies found that damage to lateral hypothalamus in rats caused aphagia, absence of eating. stimulation of it was found to elicit feeding behaviour. these effects lead researchers to conclude this was the on switch for feeding.

though the LH plays an important role in controlling eating behaviour, it is not the brains eating centre as it was found that damage also caused deficits in other aspects of behaviour such as thirst & sex rather than just hunger & more recent research showed hunger is controlled by neural circuits running throughout the whole brain.

injection of a neurotransmitter NPY into the hypothalamus of rats caused them to immediately start feeding even if satiated, producing obesity in a few days of repeated injections.

damage to the ventromedial hypothalamus caused rats to overeat, hyperphagia. stimulation of this area inhibited feeding. it was concluded that this area signals to stop eating. however, damage to this area also causes damage to the paraventricular nucleus, which is believed to cause hyperphagia alone & is responsible for our cravings.

subsequent research found that lesions to the VMH only produced overeating when they included other areas too, such as the paraventricular nucleus but others failed to replicate these findings.

IDA: much research into neural mechanisms involves animal studies, many of which can be criticised on ethical grounds for the distress they cause, not to mention the fact that they are difficult to generalise to humans, though a study has found that stimulation of the VMH in obese individuals made them feel hungry, similar to studies on rats, suggesting animal study results can be generalised to humans to some extent.

ob/ob mice receive 2 copies of gene for obesity, which are defective for the protein leptin which when normally produced by fat tissue, travels to the brain/tissues causing fat loss & decreased appetite. in ob/ob mice this doesn't happen. injecting them with leptin causes them to lose weight dramatically, illustrating the role of this particular protein in controlling weight.

AMYGDALA

thought to control selection of foods on basis of previous experience.

surgically removing the amygdala caused rats to eat both familiar & novel foods indiscriminately whereas those who still had the amygdala tended to avoid novel foods & stick to eating more familiar foods.

NEURAL MECHANISMS