A possible mechanism for repetitive stereotypic movement patterns (SMPs) in autism spectrum disorders (RAS) has been proposed. We used known data on the abnormal functioning of the neural network, including the neocortex, basal ganglia, thalamus, hippocampus and cerebellum. Taking into account the possible mechanism of functioning of this network that we proposed earlier, an analysis was carried out of the influence on its functioning of changes in the concentration of dopamine, adenosine, cannabinoids and corticoids that are characteristic of ASD. From the proposed mechanism it follows that the weakening of motor activity, one of the manifestations of which is SMPs, can be facilitated by antagonists of Gs and Gq/11 protein coupled receptors on striatoniqral cells and agonists of receptors of this type on striatopallidal cells, as well as antagonists of Gi/0 protein coupled receptors on striatopallidal cells and their agonists on striatoniqral cells. Taking into account the known data on the location of receptors on the striatal spiny cells, it follows from this mechanism that the most effective for weakening SMPs may be agonists of adenosine A2A and cannabinoid CB1 receptors, as well as antagonists of dopamine D2, histamine H3 and glucocorticoid receptors (or an effect that reduces cortisol level). When systemic using, these substances can weaken SMPs, both due to inhibition of thalamic neurons via the basal ganglia, and due to an increase in the activity of the subthalamic nucleus neurons and pyramidal neurons in the CA1 hippocampal area, the influence of which on the neocortex and amygdala prevents the shift from “cognitive” to “habitual” control of movements, which depends on the dorsal striatum. This mechanism allows to explain the strengthening and weakening of SMPs under the influence of stress and cannabinoids, respectively. The known results of clinical and experimental studies of SMPs provide evidence in favor of the proposed mechanism, which differs from those known from the literature. It may be useful in the development of new drugs for the treatment of SMPs in RAS.
I. G. Silkis (Wed,) studied this question.