Lesions in the Lateral Part of the Dorsal Parabrachial Nucleus Caused Hyperphagia and Obesity
For clarification of the role of CCK-8-like immunoreactive neurons in the lateral part of the nucleus parabrachialis dorsalis (PBD), which have fibers projecting to the ventromedial hypothalamus (VMH), the effects of unilateral and bilateral lesions in the lateral part of the PBD on increase in body...
Saved in:
Published in | Journal of Clinical Biochemistry and Nutrition Vol. 3; no. 2; pp. 103 - 112 |
---|---|
Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Gifu
SOCIETY FOR FREE RADICAL RESEARCH JAPAN
1987
Japan Science and Technology Agency |
Subjects | |
Online Access | Get full text |
Cover
Loading…
Summary: | For clarification of the role of CCK-8-like immunoreactive neurons in the lateral part of the nucleus parabrachialis dorsalis (PBD), which have fibers projecting to the ventromedial hypothalamus (VMH), the effects of unilateral and bilateral lesions in the lateral part of the PBD on increase in body weight, food and water intake, and metabolism were examined in female Sprague-Dawley rats. Unilateral and bilateral lesions caused significant increases in food and water intake, body weight gain, Lee's index, and the weights of parametrial adipose tissue, liver, and kidney. These lesions resulted in increased serum concentrations of insulin and urea, while the liver phosphoenolpyruvate carboxykinase activity tended to be decreased. These effects were quite similar to, but slightly less than, the effects of bilateral lesions of the VMH. On the side of either unilateral or bilateral lesions, the VMH did not contain CCK-8-like immunoreactive fibers. These findings support the hypothesis that the CCK-8-like immunoreactive neurons in the lateral part of the PBD send signals to the VMH and by relaying signals there they participate in the regulation of food intake and metabolism, their firing suppressing food intake and insulin secretion. However, it is also possible that the lesions induced the above changes by destroying neurons descending and ascending to other brain sites or neural fibers passing through the lesion area. |
---|---|
ISSN: | 0912-0009 1880-5086 |
DOI: | 10.3164/jcbn.3.103 |