Neurochemical aspects of the opioid-induced 'catatonia'.
In this review, the symptoms contributing to the opioid-induced 'catatonia' are presented in detail, and efforts are made to relate these symptoms to opioid-induced alterations in neurotransmitter metabolism in several parts of brain, in particular in the basal ganglia. One important symptom is the muscular rigidity, which is, at least to a great part, mediated by opioid receptors in the striatum. This effect is probably not due to an action on opioid receptors located on endings of nigro-striatal dopaminergic neurones (localization I in Fig. 2), but on receptors located on neurones, the cell bodies of which are within the striatum (localization II) or much less likely on receptors on endings of glutamergic, cortico-striatal neurones (localization IV). Another characteristic symptom, the akinesia, can be induced by injections into the nucleus accumbens, which do not lead to any significant muscular rigidity. Accordingly, opioid-induced muscular rigidity and akinesia can be dissociated topographically, and it is shown by this observation that the opioid-induced 'catatonia' is due to an interference of at least two different signs. 'Catalepsy', on the other hand, is probably the consequence of a very pronounced akinesia, and spontaneously occurring rigidity does not seem to contribute to it. In addition, opioids can induce-after low doses immediately, after high doses subsequently to the depressory phase-signs of behavioural stimulation (locomotor stimulation, some stereotypic behaviour), which seem to be antagonistic to the 'catatonia' from the functional standpoint. Several types of behavioural stimulation seem to exist, with different localizations. An activation of nigro-striatal and mesolimbic dopaminergic neurones seems to be of particular relevance in the behavioural stimulation, which is due to actions of opioids on receptors located within the substantia nigra (on endings of afferent neurones, localization III in Fig. 2) and/or within the ventral tegmentum. Part of this dopaminergic activation might be, in addition, due to actions on opioid receptors located on dopaminergic nerve endings within the striatum (localization I) or the nucleus accumbens. A hypothesis for the biphasic action of opioids (first behavioural depression, then activation is presented, involving a lower sensitivity (eg affinity) of those receptors mediating 'catatonia'. Finally, it is discussed that a detailed study of opioid action on basal ganglia might perhaps give relevant information about some pathophysiological mechanisms in schizophrenic diseases, in Parkinson's disease and in psychic dependence on opioids.
Havemann
U
U
Max-Planck-Institut für Experimentelle Medizin, Department of Biochemical Pharmacology, Göttingen, F.R.G.
Kuschinsky
K
K