Neural Mechanisms In Eating Behaviour
- Created by: Abw97
- Created on: 12-10-15 10:24
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- Neural Mechanisms In Eating beheaviour
- Homeostasis
- Mechanisms which both detect and correct the state of the internal environment to its optimal state.
- The body has 2 systems: one for turning on eating = Lateral hypothalamus and one for turning off eating: ventromedial hypothalamus
- Lateral hypothalamus
- Part of brain to turn on eating due to decrease in glucose levels. If damaged causes aphagia (stop eating). Stimulation to LH elicits eating.
- Wickens - neuropeptide Y is important in turning on eating. NPY injected into rats causes immediate eating even when satiated.
- Problems with LH as on switch
- 1. Damage to LH causes deficits in other behaviour aspects e.g. thirst and sex not just hunger.
- 2. Eating behaviour is controlled by neural circuits throughout the brain, not just the hypothalamus.
- Sakurai - 3. Although LH is plays an imortant role in controlling eating, it is not the brains eating centre.
- Problems with LH as on switch
- Wickens - neuropeptide Y is important in turning on eating. NPY injected into rats causes immediate eating even when satiated.
- Part of brain to turn on eating due to decrease in glucose levels. If damaged causes aphagia (stop eating). Stimulation to LH elicits eating.
- Ventromedial hypothalamus
- Part of brain to turn off eating due to high glucose levels. If damaged causes hyperphagia (cant stop eating) Stimulation stops feeding.
- Gold - The PVN detects the food our body needs so is responsible for craving.
- Damage to nerve fibres in VMH also damage the paraventricular nucleus. Damage to this alone causes hyperphagia.
- Gold - Damage to VMH alone did not cause hyperphagia. Overeating only happened when other areas were damaged aswell (PVN)
- However research failed to supports Golds findings ... animals which had damage to the VMH were more likely to gain weight.
- Gold - The PVN detects the food our body needs so is responsible for craving.
- Damage to nerve fibres in VMH also damage the paraventricular nucleus. Damage to this alone causes hyperphagia.
- Part of brain to turn off eating due to high glucose levels. If damaged causes hyperphagia (cant stop eating) Stimulation stops feeding.
- The role of cognitive factors.
- Amygdala = the selection of foods based on previous experiences
- Rolls and Rolls = surgically removing the amygdala in rats caused them to eat both familiar and unfamilar foods. Rats wit hamygdala would avoif unfamiliar foods.
- Kluver-Bucy Sydrome could be explained by damage to prefrontal cortex and amygdala. Patients with this sydrome show increased appetite and even attempts to eating non food items.
- Kolb and Whishaw = due to odours influences the taste of food, damage to the prefrontal cortex will decrease eating because of decline in sensory repsonce to food smell and taste.
- Kluver-Bucy Sydrome could be explained by damage to prefrontal cortex and amygdala. Patients with this sydrome show increased appetite and even attempts to eating non food items.
- Rolls and Rolls = surgically removing the amygdala in rats caused them to eat both familiar and unfamilar foods. Rats wit hamygdala would avoif unfamiliar foods.
- Inferior frontal cortex = recieves messages from the olfactory bulb (part of brain responsible for smell.
- Kolb and Whishaw = due to odours influences the taste of food, damage to the prefrontal cortex will decrease eating because of decline in sensory repsonce to food smell and taste.
- Amygdala = the selection of foods based on previous experiences
- IDA
- Reductionist - doesn't involve other explanations such as social.
- Nature/ Nurture approach
- Homeostasis
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