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Development of pre- and postsynaptic α-receptors function in the stomach of chick
2204 constant weight ~dry x~ght). The doses causing 1 g (dry weight) fecal excretion (ADt) were extrapolated from l~-dose response lines. As .~own in Table 1, 8-OH-DPAT was about 10 times more potent than buspirone in promoting defecation. Both u~amxents raised the fecal water content. The effect of 8-OH-DPAT (0.25 m g / k g s.c.) or buspirone (4 mg/kg s.c.) was dose-dependently up to completely prevented by the putative 5-HTl^-antagonist, pindolol (0.2-5 m g / k g s.c. 30 rain before), in rats chronically implanted with i.c.v, cannulae, pindolol (2.5/zg/rat i.c.v.) induced slight fecal excretion (0.3S ± 0.14 g, dry weight) and significantly prevented the effect of s.c. 8-OH-DPAT (8-OH-DPAT: 1.83 ± 0.06; p~dolol + 8-OH-DPAT: 0.42 5: 0.09; p < 001). l.c.v, injection of 8-OH-DPAT (1/zg/rat) also increased fecal output ~0.8 5: 0.1). The action of s.c. 8-OH-DPAT was not affected by ketanserin (0.2 m g / k g s.c.) and was partially prevented by atropine (0.25 mg/kg s.c.) and N-methyl-scopolamine (1 mg/kg s.c.). These results indicate that stimulation of 5-HTIA s~rotonin receptors in the CNS promote fecal excretion ~ rats and that peripheral cholinergic neurons are likely to be involved in the effector pathway.
Development of ~
and postsynapfic a-receptors function in the stomach of chick Miyazaki, H., Kawagoe T. and Taneike, T.
Deparonent of VeterinaryPharmacology, Rakuno Gakuen University, 582 Midorimachi, Bunkyodai, Ebetsu 069, Japan
The ontogenetic development of presynaptic az-adrenoceptors function is not elucidated precisely. Therefore, we studied the developmental appearance and changes of presynaptic a2-receptor function in the vagus nerve-smooth muscle preparations isolated from the chick proventriculus in associated with the changes in postsynaptic al-receptor function. The presence of presynaptic a2-receptors in these preparations have been reported (Seno et al., 1978). The motility of vagns-smooth muscle preparations isolated from chick between 9 days of incubation and 2-days after hatching was isometrically recorded in the organ bath perfusing continuously with Krebs solution. Stimulation of the vagus nerve was suppfied via a suction electrode. The stimulation of the vagus nerve (0.1-50 Hz, supramaximum voltage) caused a contraction in the preparations from 9 days of incubation. The contraction was potentiated by physostigmine (0.1 pM) and was inhibited by atropine (3 pM) or tetrodotoxin (0.67 NM), indicating that the contraction was mainly mediated by cholinergic nerves. This contraction induced by vagus nerve stimulation was inhibited by noradrenaline (Nor) in a dose-dependent manner (0.1-1 ~M) after 13 days of incubation. On the other hand, the contraction elicited by acetylcholine (5/tM) did not change by Nor. The inhibitory effects of Nor were antagonized by phentolamine (1 /tM) or an a2-antagonist, yohimbine (~ pM). Prazosin (1 ~tM), an a~-antagonist, was less effective in reducing the effects of Nor on vagally induced responses. In addition, clonidine (0.1 /tM), an a,-agonist, also inhibited the response to vagus nerve stimulation. Phenylephrine (1 pM) was less potent in inhibiting the vagally induced response. The inhibition effects of Nor tended to be larger in the responses at lower stimulus frequency (less than 10 Hz). The extent of inhibitory effects of Nor increased with the developmental ages and Nor (1 ttM) inhibited vagal responses obtained at less than 10 Hz by about 50.% after 17 days of incubation. Thus, the presynaptic a2-receptors mechanisms on the vagus nerve appeared around 13 days of incubation and get developed with the incubation period. The contraction was caused by Nor with pD z value of about 5 in longitudinal preparations after 9 days of incubation and was inhibited by phentolamine (1 pM) or prazosin (1/tM) but not tetrodotoxin (0.67/tM). Yohimbine (1/tM) was less potent in inhibiting the contraction induced by Nor. Phenylephrine (5 pM), but not clonidine (5-100 ~M) too elicited contraction. In the presence of a-blocker, Nor elicited a small relaxation in the longitudinal preparations after 17 days of incubation, which was sensitive to a /~-antagonist (carteorol, 1 /tM). Thus, the contraction mediated by a~ -adrenoceptors occurred from 9 days and the relaxation mediated by/~-receptors after 17 days of incubation. These results suggest that presynaptic a2-adrenoceptor function on the vagus nerve develops later than postsynaptic a~-receptor function on the smooth muscle of the chick proventriculus. Reference Seno et al., 1978, Eur. J. Pharmacol., 51, 229-237.
Development of ~
and postsynapfic a-receptors function in the stomach of chick Miyazaki, H., Kawagoe T. and Taneike, T.
Deparonent of VeterinaryPharmacology, Rakuno Gakuen University, 582 Midorimachi, Bunkyodai, Ebetsu 069, Japan
The ontogenetic development of presynaptic az-adrenoceptors function is not elucidated precisely. Therefore, we studied the developmental appearance and changes of presynaptic a2-receptor function in the vagus nerve-smooth muscle preparations isolated from the chick proventriculus in associated with the changes in postsynaptic al-receptor function. The presence of presynaptic a2-receptors in these preparations have been reported (Seno et al., 1978). The motility of vagns-smooth muscle preparations isolated from chick between 9 days of incubation and 2-days after hatching was isometrically recorded in the organ bath perfusing continuously with Krebs solution. Stimulation of the vagus nerve was suppfied via a suction electrode. The stimulation of the vagus nerve (0.1-50 Hz, supramaximum voltage) caused a contraction in the preparations from 9 days of incubation. The contraction was potentiated by physostigmine (0.1 pM) and was inhibited by atropine (3 pM) or tetrodotoxin (0.67 NM), indicating that the contraction was mainly mediated by cholinergic nerves. This contraction induced by vagus nerve stimulation was inhibited by noradrenaline (Nor) in a dose-dependent manner (0.1-1 ~M) after 13 days of incubation. On the other hand, the contraction elicited by acetylcholine (5/tM) did not change by Nor. The inhibitory effects of Nor were antagonized by phentolamine (1 /tM) or an a2-antagonist, yohimbine (~ pM). Prazosin (1 ~tM), an a~-antagonist, was less effective in reducing the effects of Nor on vagally induced responses. In addition, clonidine (0.1 /tM), an a,-agonist, also inhibited the response to vagus nerve stimulation. Phenylephrine (1 pM) was less potent in inhibiting the vagally induced response. The inhibition effects of Nor tended to be larger in the responses at lower stimulus frequency (less than 10 Hz). The extent of inhibitory effects of Nor increased with the developmental ages and Nor (1 ttM) inhibited vagal responses obtained at less than 10 Hz by about 50.% after 17 days of incubation. Thus, the presynaptic a2-receptors mechanisms on the vagus nerve appeared around 13 days of incubation and get developed with the incubation period. The contraction was caused by Nor with pD z value of about 5 in longitudinal preparations after 9 days of incubation and was inhibited by phentolamine (1 pM) or prazosin (1/tM) but not tetrodotoxin (0.67/tM). Yohimbine (1/tM) was less potent in inhibiting the contraction induced by Nor. Phenylephrine (5 pM), but not clonidine (5-100 ~M) too elicited contraction. In the presence of a-blocker, Nor elicited a small relaxation in the longitudinal preparations after 17 days of incubation, which was sensitive to a /~-antagonist (carteorol, 1 /tM). Thus, the contraction mediated by a~ -adrenoceptors occurred from 9 days and the relaxation mediated by/~-receptors after 17 days of incubation. These results suggest that presynaptic a2-adrenoceptor function on the vagus nerve develops later than postsynaptic a~-receptor function on the smooth muscle of the chick proventriculus. Reference Seno et al., 1978, Eur. J. Pharmacol., 51, 229-237.