Abstract
THE idea that morphine and other narcotic analgesics as well as opioid peptides affect the activity of nigrostriatal dopaminergic neurones is well supported. For instance these substances elicit changes in motor activity similar to those observed after blockade of dopamine (DA) receptors by neuroleptics, they increase DA turnover in striatum and several typical symptoms of the abstinence syndrome they provoke involve dopaminergic systems (see refs 1–3 for reviews). In agreement with these observations, a high density of ‘opiate receptors’4 and of enkephalin binding sites5,6, a high content in enkephalins7 and a dense network of enkephalin-containing neurones8 are found in the striatum. All these observations suggested the possible connection between alleged enkephalinergic neurones and the dopaminergic fibres ending in the striatum. We report here that both the regional distribution of high affinity (morphine-displaceable) binding sites for leucine-enkephalin (Leuenkephalin) in striatum and their decreased number after chemical or mechanical interruption of the nigrostriatal bundle support the assumption that enkephalinergic neurones terminate presynaptically on dopaminergic nerve terminals in the striatum.
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