Participation of noradrenergic cell groups A 1 and A2 in glucoregulation
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The body's response to glucoprivation employs such activities as increased food intake and an increased adrenal medullary response to help maintain the level of glucose in the body and brain. Noradrenergic and adrenergic neurons have been implicated in previous studies to have a role in controlling these bodily responses, but their specific roles have not been able to be picked apal1. We hypothesized that lesion of the specific noradrenergic A I and A2 neurons in the hindbrain would cause deficits in food intake tests, adrenal medullary tests and abolish the suppression of food intake controlled by satiety signals. This was tested through lesion by the neurotoxin 6-hydroxydopamine (6HD) and subsequent behavioral tests that replicated glucoprivation through the use of 2-deoxy-D-glucose (2-DG) and suppression of food intake by cholecystokinin (CCK). It was found that lesion of A I and A2 cell groups were not able to significantly decrease food intake and the blood glucose response to 2-DG, but lesion of Al neurons did cause a slower blood glucose response to 2-DG. Lesion of A2 cell groups were able to abolish the suppression of food intake by CCK. However, to better understand the role of these noradrenergic cell groups, a more effective method of administering 6HD, which is able to effectively lesion noradrenergic neurons, must be determined.