Muscarinic inhibitory transmission in mammalian sympathetic ganglia mediated by increased potassium conductance

Abstract

Slow muscarinic inhibition may be a powerful influence on membrane properties in the peripheral^1–3 and central nervous system⁴. But the location of the muscarinic receptors in sympathetic ganglia, either on interneurones or on the postganglionic membrane, and the underlying mechanism of the inhibitory response, remains controversial^5–7. In mammalian sympathetic ganglia synaptic activation of muscarinic receptors located on inhibitory interneurones was thought to release catecholamines leading to a membrane hyperpolarization called the slow inhibitory postsynaptic potential, or s.-i.p.s.p.⁸. However, the s.-i.p.s.p. in parasympathetic ganglia^3,9,10 and in amphibian sympathetic ganglia^1,2 is due to direct monosynaptic activation of muscarinic receptors, accompanied by an increased potassium conductance (but see ref. 11), and is not mediated by catecholamines. The situation is less clear in mammalian sympathetic ganglia and monosynaptic s.-i.p.s.p. observed in other ganglia could be exceptions to the hypothesis. We showed earlier that the s.-i.p.s.p. in rabbit superior cervical ganglia is not affected by catecholamine antagonists¹². We now show that the s.-i.p.s.p. in a mammalian sympathetic ganglion is due to the monosynaptic activation of muscarinic receptors, probably by an increase in potassium conductance.