Abstract:
:Early studies of hypothalamic function found that damage to the ventromedial hypothalamus (VMH) resulted in marked overeating but inferior performance in food-motivated tasks, leading several investigators to conclude that hyperphagic VMH animals were actually less hungry than normal animals. However, numerous studies have since demonstrated that under certain conditions VMH-damaged animals will work as hard or harder for food, and consume as much or more of an unpalatable diet, than normal animals. A review of these experiments suggests that most of the deficits in food-motivated behavior are the result of two dysfunctions, one obesity induced, and the other a direct result of the lesion that can be greatly alleviated by preoperative adaptation. Explanations of the VMH paradox are also examined, and it is concluded that most are too narrow in scope, generally ignoring the fact that obesity and preoperative adaptation have similar effects on thirst- and some avoidance-motivated behaviors. It is proposed that the impaired performance of VMH-lesioned animals in food-reinforced tasks is largely the result of obesity- and lesion-induced dysfunctions that are not specific to either hunger- or thirst-motivated behaviors.
journal_name
Neurosci Biobehav Revjournal_title
Neuroscience and biobehavioral reviewsauthors
King BMdoi
10.1016/0149-7634(80)90013-5subject
Has Abstractpub_date
1980-07-01 00:00:00pages
151-60issue
2eissn
0149-7634issn
1873-7528journal_volume
4pub_type
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