ROLE OF CENTRAL NICOTINIC AND BETA-ADRENERGIC RECEPTORS IN THE ONSET AND FURTHER DEVELOPMENT OF TAIL TREMOR INDUCED BY REPEATED NICOTINE ADMINISTRATION TO RATS
K. Suemaru et al., ROLE OF CENTRAL NICOTINIC AND BETA-ADRENERGIC RECEPTORS IN THE ONSET AND FURTHER DEVELOPMENT OF TAIL TREMOR INDUCED BY REPEATED NICOTINE ADMINISTRATION TO RATS, Naunyn-Schmiedeberg's archives of pharmacology, 355(5), 1997, pp. 571-575
The effects of nicotinic and beta-adrenergic receptor antagonists on t
ail-tremor induced by repeated nicotine administration were investigat
ed in rats. The daily administration of nicotine (0.5 mg/kg/day, s.c.)
for 8 days resulted in an augmentation of tail-tremor. However, repea
ted administration of dimethyl phenyl piperazinium iodide (1 mg/kg/day
, s.c.) for 8 days did not cause tail-tremor. Mecamylamine (0.5 mg/kg,
i.p), administered before the nicotine injection on each day, abolish
ed the tail-tremor. After discontinuation of the mecamylamine treatmen
t, nicotine injections caused tail-tremor augmentation. Propranolol (2
0 mg/kg, i.p.), administered before the nicotine on each day, suppress
ed the appearance of tail-tremor. After the discontinuation of propran
olol treatment, the degree of tail-tremor induced by a single injectio
n of nicotine on day 9 was much greater in the propranolol-treated gro
up than in the saline-treated control group. Neither carteolol (20 mg/
kg, i.p.) nor metoprolol (20 mg/kg, i.p.) treatment showed such effect
s, Intraspinal injection of 6-hydroxydopamine markedly enhanced the ta
il-tremor induced on the first day of nicotine injection. This effect
became more intense on subsequent administration of nicotine. The enha
nced tail-tremor following 6-hydroxydopamine treatment was abolished b
y mecamylamine (0.5 and 1 mg/kg, i.p.), and was suppressed by proprano
lol (5-20 mg/kg, s.c.) in a dose-dependent manner. These results sugge
st that central nicotinic receptors are essential for the onset and fo
r the further development of tail-tremor induced by the repeated admin
istration of nicotine, and that beta(2)-adrenoceptors are associated w
ith the tremor mechanism. Moreover, spinal noradrenergic mechanisms ma
y be involved in the manifestation of this phenomenon.