Slow inhibitory postsynaptic potentials and hyperpolarization evoked by noradrenaline in the neurones of mammalian sympathetic ganglion.

Slow IPSPs evoked in the neurones of rabbit isolated superior cervical ganglion by repetitive orthodromic stimulation, and a response evoked in the neurones of this ganglion by perfusion of noradrenaline, were studied using intracellular microelectrodes. Slow IPSPs were observed in 36% of neurones studied, and when investigated after treatment with D-tubocurarine and neostigmine, had a mean amplitude of 4.4 +/- 0.2 mV (mean +/- S.E.) and duration of 5 sec to 1.5 min. Two types of slow IPSPs occurring in different neurones were found. The slow IPSP of the first type was followed by a decrease in cell input resistance, was increased by depolarization and decreased by hyperpolarization of the membrane, with the reversal potential, if estimated by extrapolation method, equal to -77.8 +/- 3.3 mV. The slow IPSP of the second type was not followed by any change in cell input resistance, was increased by hyperpolarization and decreased by depolarization. The slow IPSP of the second type was reversibly blocked by phentolamine (1.4 X 10(-4) M). Noradrenaline (1 X 10(-4) M) evoked hyperpolarization or hyperpolarization followed by depolarization in 55% of the neurones studied. Hyperpolarization evoked by noradrenaline had a mean amplitude to 5.0 +/- 0.2 mV, was not followed by any change in cell input resistance, was reversibly blocked by phentolamine (1.4 X 10(-4) M), and was decreased by both depolarization and hyperpolarization of the cell membrane. It has been concluded that there are two groups of neurones in superior cervical ganglia, different with respect to the ionic mechanisms underlying the slow IPSP. In the first group of neurones the slow IPSP is probably due to an increase in potassium permeability of the membrane. The ionic mechanisms underlying the slow IPSP in the second group of neurones of noradrenaline-induced hyperpolarization remain unclear.