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<p>Here, a possible mechanism for repetitive stereotypic movement patterns (SMPs) in autism spectrum disorders (ASD) is 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. It follows from the proposed mechanism that the weakening of motor activity, one of the manifestations of which is SMPs, can be facilitated by action of antagonists of Gs and Gq/11 protein-coupled receptors on striatonigral cells and agonists of receptors of this type on striatopallidal cells, as well as antagonists of Gi/o protein-coupled receptors on striatopallidal cells and their agonists on striatonigral 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 administered systemically, 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 ASD.</p>

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Possible Mechanism of Repetitive Stereotypic Movement Patterns in Autism Spectrum Disorders (A Role of Neuromodulators)

  • 期刊论文

  • 发表日期：

    2025年9月1日

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  • I. G. Silkis

摘要

Here, a possible mechanism for repetitive stereotypic movement patterns (SMPs) in autism spectrum disorders (ASD) is 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. It follows from the proposed mechanism that the weakening of motor activity, one of the manifestations of which is SMPs, can be facilitated by action of antagonists of Gs and Gq/11 protein-coupled receptors on striatonigral cells and agonists of receptors of this type on striatopallidal cells, as well as antagonists of Gi/o protein-coupled receptors on striatopallidal cells and their agonists on striatonigral 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 administered systemically, 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 ASD.