title: The effects of noradrenaline on neurones in the rat dorsal motor nucleus of the vagus, in vitro.
abstract: 1. Intracellular recordings were made from vagal motoneurones identified by antidromic stimulation in the dorsal motor nucleus of the vagus (d.m.v.) in slice preparations of rat medulla oblongata. 2. Noradrenaline (NA) applied by perfusion (0.01 microM to 1 mM) depolarized 55%, hyperpolarized 32% and produced a biphasic response (hyperpolarization followed by depolarization) in 9% of the d.m.v. neurones tested. 3. The NA effects persisted after complete elimination of synaptic inputs during perfusion with Ca2+-free high-Mg2+ solution, and therefore probably resulted from a direct action on the postsynaptic membranes. 4. The NA depolarization was blocked by prazosin and the NA hyperpolarization by yohimbine, but neither was blocked by propranolol or timolol. Phenoxybenzamine blocked both responses. The results indicate that NA depolarization is mediated by alpha 1-adrenoceptors and hyperpolarization by alpha 2-adrenoceptors. 5. The neurones which were depolarized by NA were also hyperpolarized by NA when the alpha 1-adrenoceptors were blocked by prazosin (all of seven neurones tested). This result suggests that most vagal motoneurones in the d.m.v. have both alpha 1-and alpha 2-adrenoceptors. 6. The NA depolarization was accompanied by a decrease in membrane conductance and the hyperpolarization by an increase in membrane conductance, both of which were measured under manual-clamp conditions. 7. The reversal potentials for the NA responses were around -85 mV in normal Ringer solution, and shifted as predicted by the Nernst equation when the extracellular K+ concentration was changed. 8. The inhibitory postsynaptic potentials evoked by focal electrical stimulation on the slice surface of the commissural part of the nucleus of the tractus solitarius (n.t.s.), which contains an A2 catecholaminergic cell group, were abolished by yohimbine. 9. The results suggest that NA modulates vagal output by decreasing or increasing the K+ conductance of d.m.v. neurones through alpha 1- or alpha 2-adrenoceptors. In addition, the A2 noradrenergic cell group within the n.t.s. may send inhibitory inputs to the d.m.v.
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D004305:Dose-Response Relationship, Drug; D066298:In Vitro Techniques; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009046:Motor Neurons / Q000166:cytology / Q000187:drug effects*; D009638:Norepinephrine / Q000494:pharmacology*; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013569:Synapses / Q000187:drug effects; D014630:Vagus Nerve / Q000187:drug effects*
chemical_list: D000317:Adrenergic alpha-Antagonists; D008274:Magnesium; D011188:Potassium; D009638:Norepinephrine