Sympathetic transmission to the dilator muscle of the rat iris.

The responses of the dilator layer of the rat iris to sympathetic nerve stimulation were examined using intracellular recording techniques. Three different cell types were detected. In two of these, which were assumed to reflect recordings from myoepithelial cells, sympathetic nerve stimulation initiated excitatory junction potentials. These started after a delay of several hundred milliseconds and lasted for several seconds. The excitatory junction potentials were abolished by low concentrations of prazosin and were relatively insensitive to yohimbine, indicating that neurally released noradrenaline activated an alpha 1-adrenoceptor. The adrenoceptor was further characterised as being of the alpha 1b subtype using chlorethylclonidine. The time course of excitatory junction potentials was slowed when the preparation was cooled, suggesting that a second messenger pathway was being activated. The contractions triggered by sympathetic nerve stimulation persisted after excitatory junction potentials had been abolished by reducing the external concentration of chloride ions and after adding the organic calcium antagonist, nifedipine. Thus it seems likely that contractions of the dilator are triggered by the release of calcium ions from internal stores. These observations are discussed in relation to the idea that alpha 1b-adrenoceptors are coupled to a messenger pathway which involves inositol triphosphate and the pulsatile release of calcium ions from internal stores. The second section of the paper deals with the structure of neuro-myoepithelial contacts in the dilator layer. The majority of sympathetic varicosities formed organized neuroeffector junctions with either myoepithelial cells or melanophores. At the junctions the effector cell membrane and varicosity membrane were separated by less than 80 nm, with synaptic vesicles concentrated towards the neuroeffector junction. The synaptic vesicles in varicosities that failed to form junctions did not aggregate towards their regions of exposed membrane. These observations are discussed in relation to the idea that transmission at autonomic varicosities occurs at organised neuroeffector junctions.