Abstract
The effects of stimulation of guinea pig superior cervical ganglia (SCG) in vitro with 50 μM concentrations of dopamine, L-norepinephrine or L-isoproterenol in Eagle's Medium containing 5 mM theophylline were determined. Dopamine (50 μM) produced no stimulation of cyclic AMP levels, 50 μM norepinephrine produced a doubling of cyclic AMP levels, while 50 μM isoproterenol produced a 6-fold increase in cyclic AMP levels over control values. The increases were blocked by propranolol, indicating that they were due to stimulation of a β-adrenergic receptor-adenylate cyclase complex. In the rabbit SCG, by contrast, 50 μM dopamine produced an increase in cyclic AMP levels of 60% over control values. The possible involvement of the β-receptor complexin the modulation of ganglionic transmission was tested by subjecting ganglia to supramaximal stimulation for 8 min. No elevation of cyclic AMP levels occured in guinea pig SCG, but a doubling of cyclic AMP levels in rabbit SCG was noted. Current concepts of the function of cyclic AMP in neural transmission in the SCG involve a dopaminergic SIF cell, dopamine receptor-adenylate cyclase complex, and the generation of a slow inhibitory postsynaptic potential (s-IPSP). Previous research has indicated that the guinea pig SCG lacks a s-IPSP, and its SIF cells contain norepinephrine rather than dopamine. Since preganglionic stimulation of the guinea pig SCG has now been shown not to cause increased cyclic AMP levels, and since the cyclic AMP content of the guinea pig SCG is not increased following incubation with dopamine, we conclude that a dopamine receptor-adenylate cyclase complex is not involved in the modulation of neural transmission in the guinea pig SCG.
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