Effects of noradrenaline on rat paratracheal neurones and localization of an endogenous source of noradrenaline.

1. Intracellular recording techniques were used to study the actions of exogenous noradrenaline (NA) on rat paratracheal neurones in situ. The receptor subtypes underlying these actions were investigated by application of selective adrenoceptor antagonists. 2. Application of NA (0.1-10 microM) by superfusion evoked a membrane depolarization in 85% (52 out of 61) of all paratracheal neurones studied. The response consisted of a slow depolarization which was sometimes accompanied by action potential discharge. In 26 out of 31 cells the response was associated with a change in input resistance of the cell membrane. In 22 out of 26 cells there was a 30% increase, whilst in a further 4 cells there was a 15% decrease in input resistance. The amplitude of the NA depolarization was concentration-dependent. 3. The depolarization evoked by NA was reversibly antagonized by prazosin (1 microM) but unaffected by yohimbine (1 microM) or propranolol (1-10 microM). 4. High performance liquid chromatography with electrochemical detection (h.p.l.c.-e.c.d.) was used to assay for NA and dopamine in samples containing mainly paratracheal ganglia and in samples of tracheal smooth muscle with mucosa. NA was present in all samples assayed at a level of 1.6 micrograms NA g-1 and 0.5 microgram NA g-1 wet weight of the two sample types respectively. Dopamine was not detected in any samples of either ganglia or smooth muscle with mucosa. 5. It is concluded that NA-evoked depolarizations of rat paratracheal neurones result from stimulation of alpha 1-adrenoceptors, and that local levels of NA may be sufficiently high to activate these receptors directly.