Abstract
Electrical stimulation of mouse vasa deferentia or of rat occipital cortex slices which were previously incubated with 3H-(-)noradrenaline [norepinephrine, NE] increased the overflow of tritium from the tissue above that occurring spontaneously. Phentolamine (10 .mu.M) increased evoked tritium overflow from vasa deferentia as did both phentolamine and yohimbine (1.25 .mu.M) when applied to cortex slices. Evoked tritium overflow from cortex slices was increased by cocaine (20 .mu.M) but neither cocaine (11 .mu.M) nor desmethylimipramine (0.5 .mu.M) increased evoked tritium overflow significantly in the vas deferens. In contrast to its effect when applied alone, in the presence of phentolamine, cocaine produced a further increase in evoked tritium overflow in both tissues. Application of (-)-NE in the presence of cocaine produced a reduction in evoked tritium overflow which was quantitatively similar in both tissues. The effect on tritium overflow of blockade of the reuptake of NE by cocaine is apparently masked in mouse vas deferens by a compensatory process mediated through presynaptic .alpha.-adrenoreceptors. It may be that such a compensation does not occur in cortex slices because of a difference in the architecture of the synapse in this tissue.