AN INVESTIGATION OF THE ROLE OF GANGLIA IN THE INNERVATION OF THE RAT ANOCOCCYGEUS MUSCLE: AN ELECTRICAL AND MECHANICAL STUDY

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Abstract
A preparation is described which allows the rat anococcygeus muscle to be stimulated via its two extrinsic nerves. Each nerve contains both excitatory and inhibitory fibres. A ganglionated nerve plexus lies on the surface of the muscle. The possibility that at least part of the excitatory pathway was interrupted by a ganglion synapse lying in one of the nodes of plexus close to the muscle was suggested by the observations that (a) the excitatory response to extrinsic nerve stimulation was reduced by the nicotinic antagonists tubocurarine (0.13 to 0.26 mm) and dihydro β‐erythroidine (0.1 to 0.14 mm), (b) Fibres from one extrinsic nerve were shown to synapse on a ganglion cell from which intracellular recordings were made while the output from this ganglion cell was traced microscopically to the muscle. Intracellular recording from ganglion cells in this plexus indicated that cholinergic synaptic transmission occurred in these ganglia. Tubocurarine (0.13 mm) and hexamethonium (1.3 mm) reversibly abolished intracellularly‐recorded synaptic potentials. Hexamethonium (0.1 to 1 mm) initially enhanced the motor response to nerve stimulation and raised muscle tone, probably by an action involving pre‐ and postsynaptic sites. Subsequently, hexamethonium inhibited the response to extrinsic nerve stimulation presumably by an effect at ganglia lying along the excitatory pathway. Hexamethonium enhanced, without subsequently inhibiting, the response to exogenously added noradrenaline in both untreated and 6‐hydroxydopamine‐treated rats. These results suggest that the initial enhancement produced by hexamethonium involved sites at postganglionic nerve endings and on smooth muscle receptors. Inhibitory responses were obtained following extrinsic nerve stimulation when the tone of the muscle was raised and the excitatory response abolished by either guanethidine (3 μm) alone or by carbachol (10 μm) followed by phentolamine (3 μm). The inhibitory response was not reduced by hexamethonium (up to 2.8 mm) tubocurarine (up to 1.3 mm) or by atropine (up to 1 μm).