Membrane currents underlying the cholinergic slow excitatory post‐synaptic potential in the rat sympathetic ganglion.

Abstract

SUMMARY1. Non-nicotinic slow synaptic currents were recorded from voltage-clamped neurones in isolated rat superior cervical ganglia bathed in a solution containing d-tubocurarine and (usually) 1 /LM-neostigmine.2. Three components ofslow synaptic current could be detected following repetitive preganglionic stimulation: a net inward current resulting from inhibition of the voltage-dependent outward K+ current IM; a net outward current associated with a fall in membrane conductance when IM was deactivated by membrane hyperpolarization or inhibited with external Ba2+ or internal Cs+; and an occasional late inward current associated with an increased membrane conductance. As a result, synaptic current amplitudes showed complex changes with changes in membrane potential.3. Both the inward current associated with IM inhibition and the outward current were enhanced by neostigmine and blocked by atropine or pirenzepine, and therefore resulted from activation of muscarinic receptors.4. In unclamped neurones, equivalent stimulation produced a membrane depolarization and induced or facilitated repetitive spike discharges.5. It is concluded that the principal synaptic response to muscarinic receptor activation is IM inhibition, leading to a net inward current and increased excitability, but that this response may be modified under certain circumstances by other synaptic currents.

Burst‐patterned stimulation promotes nicotinic transmission in isolated perfused rat sympathetic ganglia.

“…Under the stimulus conditions used here, which activated only small numbers of preganglionic fibres, the slow synaptic events studied in detail in rat SCG by Brown & Selyanko (1985) were present in only five of all the cells studied, and then only at stimulation frequencies of 10 Hz and greater. In the rest of the cells, membrane potential and input resistance remained constant throughout the range of stimulation frequencies.…”

The α Subunit of GqContributes to Muscarinic Inhibition of the M-Type Potassium Current in Sympathetic Neurons

“…Thus, cells remain clamped around rest, display spike adaptation, and have limited excitability. Inhibition of I K(M) results in depolarization with increased action potential discharge (Brown and Selyanko, 1985) and provides a switch between phasic and tonic firing properties (Wang and McK innon, 1995). I K(M) in rat SCG neurons can be inhibited after activation of various receptors, including M 1 muscarinic receptors [M 1 mAChR Bernheim et al, 1992)] and bradykinin B 2 receptors , coupled through Bordetella pertussis toxin-insensitive GTPbinding proteins (G-proteins) Caulfield et al, 1994;Jones et al, 1995).…”

Ca2+ signal summation and NFATc1 nuclear translocation in sympathetic ganglion neurons during repetitive action potentials

“…Application of the K + channel blocker Ba 2+ induced repetitive, partially summating Ca 2+ transients in the initially non-repetitive neuron (Figure 4 A, red records), and increased the frequency and number of Ca 2+ transients in the initially repetitively responding neuron (Figure 4 B, red records). Extracellular application of the K + channel blocker Ba 2+ is commonly used to inhibit M-type K + currents [17,18]. In addition, in sympathetic neurons Ba 2+ has been shown to induce strong SFF [10].…”