SYMPATHETIC INPUT TO GANGLIA OF THE GUINEA-PIG SPHINCTER OF ODDI

Intracellular recording and immunohistochemical staining techniques we re used to establish whether sphincter of Oddi (SO) ganglia are a targ et of sympathetic input to this region. Norepinephrine (0.01-10.0 mu M ) decreased the amplitude of the nicotinic fast excitatory postsynapti c potential (EPSP) evoked by stimulation of interganglionic fiber trac ts, with a half-maximal inhibitory concentration (EC(50)) of 300 nM. N orepinephrine did not alter the responsiveness of the neurons to acety lcholine. The alpha(2)-adrenoreceptor agonist UK-14304 mimicked the no repinephrine-induced effect with a EC(50) 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 mu M) inhibited the UK-1430 4 response, with a dissociation constant of 1.0 nM. Release of endogen ous catechol- amines, by the addition of tyramine (100 mu M) to the ba th, caused an idazoxan-sensitive decrease in the amplitude of the fast EPSP. In the minority of SO neurons that exhibited inhibitory postsyn aptic potentials (IPSPs), norepinephrine caused a hyperpolarization of the membrane potential. The IPSP and the norepinephrine-induced hyper polarization were inhibited by alpha(2)-adrenoreceptor antagonists. De sipramine (1.0 mu M), an uptake inhibitor, reversibly increased the am plitude of the IPSP. Immunoreactivities for tyrosine hydroxylase and d opamine beta-hydroxylase were coexistent in nerve fibers and nonexiste nt in cell bodies in the ganglionated plexus of the SO. The results of this study indicate that norepinephrine acts pre- and postsynapticall y as an inhibitory neurotransmitter in SO ganglia.