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Catecholamine turnover in rats with ventromedial hypothalamic lesions.
The American Journal of Physiology
|April 1, 1984
Summary
Ventromedial hypothalamic (VMH) lesions in rats increase norepinephrine turnover in the heart and brown adipose tissue. However, these lesions prevent the normal slowing of norepinephrine turnover during fasting.
Area of Science:
- Neuroscience
- Physiology
Background:
- The ventromedial hypothalamus (VMH) plays a crucial role in regulating autonomic functions.
- Norepinephrine (NE) is a key neurotransmitter involved in thermogenesis and metabolic regulation.
Purpose of the Study:
- To investigate the impact of VMH lesions on norepinephrine turnover in specific tissues.
- To understand how VMH lesions affect the response of NE turnover to physiological challenges like fasting and cold exposure.
Main Methods:
- Rats with VMH lesions and sham-operated controls were studied.
- Norepinephrine synthesis was blocked using alpha-methyl-p-tyrosine to measure NE turnover.
- Measurements were taken in brown adipose tissue, heart, and pancreas under ad libitum feeding, pair-feeding, fasting, and cold exposure conditions.
Main Results:
- VMH lesions significantly increased NE turnover in brown adipose tissue and heart two weeks post-lesion, regardless of feeding conditions.
- No effect of VMH lesions on pancreatic NE turnover was observed.
- Fasting slowed NE turnover in control rats but had a diminished effect in VMH-lesioned rats.
- Cold exposure increased NE turnover in both groups, with no significant difference between VMH-lesioned and control rats.
Conclusions:
- VMH lesions alter sympathetic nervous system activity, particularly affecting norepinephrine turnover in metabolically active tissues.
- The data suggest a disruption in the autonomic regulation of energy balance following VMH lesions, especially concerning the response to fasting.