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Nicotine-induced tail-tremor and drug effects
Y Gomita1, K Suemaru, K Furuno
1Department of Hospital Pharmacy, Okayama University Medical School, Japan.
Pharmacology, Biochemistry, and Behavior
|December 1, 1989
Summary
Nicotine administration in rats causes tail tremors, which are blocked by mecamylamine but not other drugs. This suggests nicotine
Area of Science:
- Neuroscience
- Pharmacology
- Behavioral Science
Background:
- Nicotine is a psychoactive alkaloid found in tobacco.
- Nicotine exerts its effects through various receptor systems in the central and peripheral nervous systems.
- Understanding nicotine's effects is crucial for addiction research and smoking cessation strategies.
Purpose of the Study:
- To investigate the development of tail-tremor response to repeated nicotine administration in rats.
- To examine the effects of various pharmacological agents on nicotine-induced tail-tremor.
- To elucidate the receptor mechanisms underlying nicotine-induced tail-tremor.
Main Methods:
- Male Wistar rats were administered nicotine subcutaneously (0.5 mg/kg) six times daily.
- The onset, peak, and duration of tail-tremor were recorded.
- The effects of mecamylamine, arecoline, atropine, scopolamine, hexamethonium, and physostigmine on nicotine-induced tail-tremor were evaluated.
Main Results:
- Repeated daily nicotine administration induced tail-tremors starting on the third day.
- The tremor response showed tolerance within the day but increased with daily injections.
- Mecamylamine abolished nicotine-induced tail-tremor, while other tested drugs did not.
- Physostigmine potentiated the tremor response.
Conclusions:
- Nicotine-induced tail-tremor in rats is a reproducible phenomenon.
- The results suggest that central nicotinic acetylcholine receptors mediate nicotine-induced tail-tremor.
- Mecamylamine's blockade indicates the involvement of nicotinic receptors in this response.