𝔖 Bobbio Scriptorium
✦   LIBER   ✦

Tail-pinch-induced hyperphagia in weanling rats with dorsomedial hypothalamic lesions

✍ Scribed by Lee L. Bernardis; Larry L. Bellinger; Jack K. Goldman


Publisher
John Wiley and Sons
Year
1980
Tongue
English
Weight
554 KB
Volume
5
Category
Article
ISSN
0360-4012

No coin nor oath required. For personal study only.

✦ Synopsis


Abstract

Dorsomedial hypothalamic lesions (DMNL) were produced in 26‐day‐old and 44‐day‐old male rats. Sham‐operated rats served as controls. Tail‐pinching (TP) was performed for five minutes at a time over two periods: the first TP period of six sessions each from post‐operative day 1 to day 17 and the second TP period of eight sessions from post‐operative day 18 to day 35. Three equicloric diets, high‐carbohydrate, high‐fat, and high‐protein, were presented ad libitum in pellet form during the TP sessions. Lab chow was available ad libitum in the home cages. Rats with DMNL at age 26 days did not show TP‐induced hyperphagia and HCD preference compared to the controls until the second TP period. In rats lesioned at age 44 days, TP‐induced hyperphagia and HCD‐preference (compared with controls) became evident immediately after the operation. In the home cages (lab chow), DMNL rats showed a decline in food intake from the first to the second TP period, while the sham‐operated controls showed an increase. TP‐induced hyperphagia in the rat with DMNL does not appear to be caused by some arousal‐related process as has been shown for the rat with lateral hypothalamic lesions. Lesions in the nigrostriatal system have been reported to attenuate TP‐induced feeding, while the present study indicates that lesions in the DMN enhance it. This suggests that fibers in the central nervous system may be involved in facilitation or inhibition of TP‐induced eating.


📜 SIMILAR VOLUMES


Hepatic enzyme activities in weanling ra
✍ Dr. Lee L. Bernardis; Fred Rosen; Jack K. Goldman; Roy Martin 📂 Article 📅 1977 🏛 John Wiley and Sons 🌐 English ⚖ 706 KB

## Abstract Weanling rats received bilateral electrolytic lesions in the ventromedial (VMN) or dorsomedial (DMN) hypothalamic nuclei; sham‐operated rats served as controls. The animals were maintained under standard conditions for 13–;17 days post‐operatively and killed by decapitation. In addition

Glucose preference and caloric regulatio
✍ Dr. Lee L. Bernardis; John R. Border 📂 Article 📅 1975 🏛 John Wiley and Sons 🌐 English ⚖ 485 KB

## Abstract Weanling male rats received electrolytic lesions in the ventromedial (VMN) and dorsomedial (DMN) hypothalamic nuclei, respectively. A third group of rats served as sham‐operated controls (CON). After the two hypothalamic syndromes had been well established, the animals were subjected to

Relative normophagia and organ growth in
✍ Dr. Lee L. Bernardis; Larry L. Bellinger 📂 Article 📅 1979 🏛 John Wiley and Sons 🌐 English ⚖ 464 KB

Weanling rats with ventromedial (VMNL) and dorsomedial (DMNL) hypothalamic lesions and sham-operated controls were maintained up t o 198 days after operation. Food intake was measured throughout the experiment and organ weights were recorded at various periods of sacrifice. Comparisons were made bet

Failure to demonstrate alterations in gl
✍ Dr. Lee L. Bernardis; Jack K. Goldman; Larry L. Bellinger 📂 Article 📅 1976 🏛 John Wiley and Sons 🌐 English ⚖ 530 KB

## Abstract Bilateral electrolytic lesions were placed in the dorsomedial hypothalamic nuclei (DMN) of weanling male Sprague‐Dawley rats. Sham‐operated rats served as controls. After 22 days on lab chow and tap water ad libitum, the animals were injected with U‐^14^ C‐alanine 0.167 μC/μ moles intra

Food intake of weanling rats with lesion
✍ Dr. Lee L. Bernardis; John R. Border 📂 Article 📅 1975 🏛 John Wiley and Sons 🌐 English ⚖ 639 KB

## Abstract Male rats received bilateral electrolytic lesions shortly after weaning in the ventromedial (VMN) and dorsomedial (DMN) hypothalamic nuclei, respectively. A third group of rats served as sham‐operated controls. The animals were subjected to intragastric preloading with 33% d‐glucose and