Enhancement of peptidergic synaptic transmission by catecholamines in the bullfrog sympathetic ganglion.

Extracellular recordings were made from postganglionic branches or ganglion cells of the 9th or 10th ganglia of the paravertebral sympathetic chain of the bullfrog in vitro. Tetanic preganglionic stimulation, applied to nerve fibers between the 7th and 8th ganglia, elicited cholinergic (muscarinic) and non-cholinergic synaptic responses in nicotinized preparations. These were an early after-discharge (EAD) and a late after-discharge (LAD), respectively. Brief application (3-10 min) of catecholamines augmented the LAD and this augmentation continued for 90-120 min after catecholamine withdrawal. In contrast, these catecholamines did not significantly augment the EAD. The catecholamine effects were concentration-dependent within the range 1-100 microM, and the order of the potency was isoprenaline greater than adrenaline greater than noradrenaline greater than dopamine = phenylephrine. The catecholamine-induced augmentation was blocked by propranolol (0.1-1 microM) and pindolol (1-10 microM), but not by phentolamine (up to 10 microM). The catecholamine-evoked augmentation of the LAD could be mimicked by dibutyryl cyclic adenosine 3',5'-monophosphate (dbc-AMP) at 1-50 microM. However, similar concentrations of cyclic adenosine 3',5'-monophosphate (c-AMP), cyclic guanosine 3',5'-monophosphate (c-GMP) and dibutyryl c-GMP (dbc-GMP) had no effect. None of cyclic nucleotides appreciably augmented the EAD. Methylxanthines, 3-isobutyl-1-methylxanthine and caffeine, facilitated the LAD and potentiated the isoprenaline-induced augmentation of the LAD. The excitatory actions of luteinizing hormone releasing hormone (LHRH) were also enhanced by (-)-isoprenaline and dbc-AMP. The former was prevented by propranolol.(ABSTRACT TRUNCATED AT 250 WORDS)