1. Spontaneous, in vivo synaptic activity was recorded from 146 B‐cells and 60 C‐cells in the IXth and Xth paravertebral sympathetic ganglia of the urethane‐anaesthetized bullfrog. Sympathetic outflow to the blood vessels, which are innervated by C‐cells, is different from that received by targets in the skin, which are innervated by B‐cells. 2. B‐cells were divided into three groups: the first (61 cells) exhibited only action potentials (APs) at 0.01‐0.3 s‐1; the second (59 cells) exhibited APs and EPSPs and the third (26 cells) were silent. In addition to their usual suprathreshold input from the ipsilateral sympathetic chain, 53% of B‐cells received subthreshold input which probably arose from fibres in the contralateral chain. ‘Slow’ B‐cells exhibited less subthreshold activity and a slightly higher AP frequency than ‘fast’ B‐cells. All B‐cells are involved in a sympathetic reflex which is activated by tactile stimulation of the skin of the hindlimb. Activation of this reflex increased AP frequency without promoting long‐lasting depolarization. 3. Sixty‐seven per cent of C‐cells exhibited rhythmic bursting activity with or without small intraburst EPSPs. Bursts tended to correlate with electrocardiographic (ECG) activity. The remainder exhibited an irregular pattern of activity which was not correlated with ECG activity and which included one to three APs and EPSPs interspersed between the bursts. Activity of both types of C‐cell was inhibited following stimulation of the skin. 4. An average of twenty‐three B‐cells and twenty‐one C‐cells discharge simultaneously in vivo. This reflects branching of preganglionic fibres and results in synchrony of discharge in both postganglionic B‐ and C‐fibres.(ABSTRACT TRUNCATED AT 250 WORDS)

Synaptic activity of individual B and C cells in the paravertebral sympathetic ganglia of urethan-anesthetized bullfrogs was monitored with intracellular electrodes. Postganglionic activity from the B and C fiber populations was monitored with suction electrodes. Intravenous infusion of muscarine (0.1 ml of 8 microM) excited individual B cells and increased the amplitude and rate of spontaneous, postganglionic B fiber population discharges. Muscarine also increased the number of action potentials (APs) within each burst of synaptic activity in individual C cells. Because atropine (0.1 ml of 0.1 microM) had little or no effect on postganglionic population B or C fiber activity, the muscarinic slow inhibitory postsynaptic potentials and slow excitatory postsynaptic potentials (EPSPs) are unlikely to be involved in the transmission, modulation, or integration of postganglionic outflow in vivo. Atropine did, however, decrease the number of APs per burst in individual C cells, an effect that could be explained if excitatory presynaptic muscarinic receptors exist on C fiber terminals. Stimulation of preganglionic C fibers at "physiological" frequencies evoked a lasting afterdischarge in postganglionic B fibers that was blocked by a combination of atropine and [D-pyro-Glu1,D-Phe2,D-Trp3,6]-luteinizing hormone-releasing hormone (LHRH). Release of LHRH from C fiber terminals and activation of the peptidergic, late-slow EPSP mechanism in B cells may therefore play a role in ganglionic transmission in vivo.

A 2 min sample of an intracellular recording of in vivo synaptic activity from a vasomotor C-neuron in a bullfrog sympathetic ganglion was converted to a series of stimulus pulses. This physiologically derived activity was used to stimulate preganglionic C-fibres of similar ganglia studied in vitro. Intracellular recordings were made from exocrine B-cells within the ganglia. Although they do not receive fast, nicotinic synaptic input from preganglionic C-fibres, B-cell excitability was profoundly increased by stimulation of C-fibres with physiologically derived activity. Also, subthreshold depolarizing current pulses that failed to generate action potentials in B-cells under control conditions almost always generated action potentials whilst C-fibres were activated. These effects were attenuated or prevented by the luteinizing hormone releasing hormone antagonist, [D-pyro-Glu1,D-Phe2,D-Trp3,6]-LHRH (70 microM). The physiological release of luteinizing hormone releasing hormone from C-fibres therefore causes an interaction between vasomotor and exocrine outflow within a paravertebral sympathetic ganglion.

A 2 min sample of an intracellular recording of in vivo synaptic activity from a vasomotor C-neuron in a bullfrog sympathetic ganglion was converted to a series of stimulus pulses. This physiologically derived activity was used to stimulate preganglionic C-fibres of similar ganglia studied in vitro. Intracellular recordings were made from exocrine B-cells within the ganglia. Although they do not receive fast, nicotinic synaptic input from preganglionic C-fibres, B-cell excitability was profoundly increased by stimulation of C-fibres with physiologically derived activity. Also, subthreshold depolarizing current pulses that failed to generate action potentials in B-cells under control conditions almost always generated action potentials whilst C-fibres were activated. These effects were attenuated or prevented by the luteinizing hormone releasing hormone antagonist, [D-pyro-Glu1,D-Phe2,D-Trp3,6]-LHRH (70 microM). The physiological release of luteinizing hormone releasing hormone from C-fibres therefore causes an interaction between vasomotor and exocrine outflow within a paravertebral sympathetic ganglion.

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