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Increase of pineal noradrenaline concentration in rats by desipramine but not fluoxetine: implications concerning the specificity of these uptake inhibitors

Reuptake across the neuronal membrane appears to be the major mechanism by which neurotransmitter monoamines are inactivated after release into the synaptic cleft. This neuronal reuptake process is readily demonstrated in brain slices or in synaptosomes in vitvo. Some inhibitors of amine uptake are remarkably selective in blocking the uptake of 5-hydroxytryptamine (5-HT) or noradrenaline. For example, desipramine is a selective inhibitor of noradrenaline uptake, whereas fluoxetine is a selective inhibitor of 5-HT uptake in virro and in vivo (Fuller & Wong, 1977). A question that sometimes arises is whether the selectivity of an uptake inhibitor relates to the uptake pump or to the substrate. That is, does fluoxetine inhibit uptake of any amine by the pump on 5-HT neuronal membranes? Or, does fluoxetine inhibit 5-HT uptake, whether that uptake is by 5-HT neuronal membrane pumps or by other pumps, such as on catecholamine neurons'? The latter question becomes important in interpreting certain pharmacological experiments. For instance, when 5-hydroxytryptophan is injected, some of it may be decarboxylated to 5-HT in cells other than 5-HT neurons. If it is decarboxylated in catecholamine neurons, the 5-HT so formed may influence their functioning either by displacing some catecholamine from storage granules or by being released as a false neurotransmitter. If an uptake inhibitor is specific for a neuronal pump, then enhancement by fluoxetine of some effect of injected 5-hydroxytryptophan can properly be interpreted as indicating that action is mediated by 5-HT neurons. There are probably few instances in which an amine is taken up physiologically by a neuronal pump other than the one on the neuron that released that amine. One situation in which 5-HT is taken up by noradrenaline neurons under physiological conditions appears to be in the pineal gland (Jaim-Etcheveiry & Zieher, 1968). Noradrenaline nerve fibres innervate the pineal gland, releasing noradrenaline and re-taking it up as a means of terminating its action on receptor sites on the pineal cells. The pineal cells synthesize large quantities of melatonin, with 5-HT as an intermediate. Because the concentrations of 5-HT in the pineal gland are large compared with those of noradrenaline, the uptake pumps on the noradrenaline nerve membrane 'accidentally' suck in substantial quantities of 5-HT along with the noradrenaline. This systema noradrenaline pump taking up 5-HTprovides an uncommon opportunity to study the specificity of an uptake inhibitor. Which