Sympathetic input to ganglia of the guinea pig sphincter of Oddi.

Intracellular recording and immunohistochemical staining techniques were used to establish whether sphincter of Oddi (SO) ganglia are a target of sympathetic input to this region. Norepinephrine (0.01-10.0 microM) decreased the amplitude of the nicotinic fast excitatory postsynaptic potential (EPSP) evoked by stimulation of interganglionic fiber tracts, with a half-maximal inhibitory concentration (EC50) of 300 nM. Norepinephrine did not alter the responsiveness of the neurons to acetylcholine. The alpha 2-adrenoreceptor agonist UK-14304 mimicked the norepinephrine-induced effect with a EC50 of 2.5 nM, whereas alpha 1- and beta-adrenoreceptor agonists had no effect on the EPSP. The alpha 2-adrenoreceptor antagonist idazoxan (1.0 microM) inhibited the UK-14304 response, with a dissociation constant of 1.0 nM. Release of endogenous catecholamines, by the addition of tyramine (100 microM) to the bath, caused an idazoxan-sensitive decrease in the amplitude of the fast EPSP. In the minority of SO neurons that exhibited inhibitory postsynaptic potentials (IPSPs), norepinephrine caused a hyperpolarization of the membrane potential. The IPSP and the norepinephrine-induced hyperpolarization were inhibited by alpha 2-adrenoreceptor antagonists. Desipramine (1.0 microM), an uptake inhibitor, reversibly increased the amplitude of the IPSP. Immunoreactivities for tyrosine hydroxylase and dopamine beta-hydroxylase were coexistent in nerve fibers and nonexistent in cell bodies in the ganglionated plexus of the SO. The results of this study indicate that norepinephrine acts pre- and postsynaptically as an inhibitory neurotransmitter in SO ganglia.