Created by freycameron
over 10 years ago
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Question | Answer |
:) Anand & Brobeck (1951) AO2 (LH) | -A lesion in the LH led to aphagia in rats -Backed up by studies where electrical stimulation of LH produced feeding behaviour in rats |
:( However... (AO2) | -Not just an on switch for eating; controls other behaviours too -Eating behaviour controlled by neural circuits, not just hypothalamus -Furthermore, the effects of lesioning the LH were only temporary, suggesting that it is not the only 'on' switch |
:) Stanley et al (1986) AO2 | -Repeated injections of NPY into hypothalamus of rat produces obesity in a few days -:) because research is scientific; cause & effect etc. |
:) AO2 (VMH) | -Lesions or damage to VMH resulted in hyperphagia and obesity -Therefore controls eating behaviour |
:( Gold (1973) AO2 (VMH) | -Lesions restricted to the VMH alone did not result in hyperphagia and only produced overeating when they included other areas such as the paraventricular nucleus -However, subsequent studies have failed to replicate this, and have found that animals with damaged VMH ate substantially more and gained more weight |
:) Physiological research AO2 | -Damage to amygdala could explain feeding abnormalities observed in Kluver-Bucy syndrome -This causes increased appetite, indiscriminate eating, and attempts to eat non-food items |
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