Disorders cerebellar-cortical pathways associated with autistic behavior

In mice with autistic spectrum disorder revealed impaired functional connections between medial prefrontal cortex and the cerebellum. As stated in the article, published in Nature Neuroscience, this relationship starts from the cortex of the hemispheres and of the worm of the cerebellum goes through the nuclei of the cerebellum, and the ventromedial thalamus and ends in the medial prefrontal cortex of the large hemispheres of the brain. When activated, this road mice showed the classic symptoms of the disorder: less interacted with the other dogs and did repetitive actions. In contrast, stimulation of neurons lunate lobules of the cerebellum reduced antisocial behavior, and the activation of neurons in the posterior part of the cerebellar vermis eliminated repetitive behavior in male mice. Changes of brain structures through which this path was observed in people with autism spectrum disorder.

The exact causes of autism spectrum disorder (ASD) nobody knows. In the material “Children of rain” we talked about some risk factors that can lead to the development of this disorder. It may appear differently, however, two major symptoms, allowing the physician to suspect the disorder in a child is a difficulty in communication and repetitive actions. For example, a child can spend hours spinning office chair non-stop, but can not maintain a simple conversation. In adulthood, this is manifested by the lack of even basic empathy and separation of interests of the partner in communication.

Neurophysiological basis of RACES is also still poorly understood. A number of studies indicates that the contribution of cerebellar dysfunction to the development of autism symptoms in mice, including those due to deletions of the gene Tsc1 in Purkinje cells. In many studies was described in detail volumetric change in the back of the worm and Crescent in the upper lobe in children with ASD; however, they correlated with the severity of the disorder.

Peter Tsai (Peter T. Tsai) with colleagues from the southwestern medical center the University of Texas decided to check, does the violation of the activity of the cerebellum to work the medial prefrontal cortex — the brain region that manages cognitive functions in mice with mutation in the gene Tsc1 in Purkinje cells. Scientists have suggested that in these mice the relationship between the upper Crescent slice of the cerebellum and the left preliminay region of the medial prefrontal cortex may be disrupted.

To examine the degree of correlation between the damaged structures and manifestations of the RAS in mice, the researchers used the method of structural covariance. This method is based on image analysis of functional or diffusion MRI sections of the brain. In the study group of 94 mouse lines with mutations in genes associated with ASD, the researchers found disrupted structural covariance between the upper Crescent slice of the cerebellum and the left preliminay region of the medial prefrontal cortex in mice with ASD compared to the control group (p < 0.05).

The scientists also found a higher frequency of the single spikes in the left preliminay region of the medial prefrontal cortex in mice with RAS (p < 0.0001). This pattern indicates a decrease in the inhibitory effects of the mutant cerebellum and increased descending activity of the medial prefrontal cortex.

To understand what other structures affecting the studied way in mice, scientists applied the methods of fluorescent staining. They found that the axons of Purkinje cells located in the upper lobe lunate, toothed go to the core of the cerebellum. In addition, when geograficheskom inhibition of neurons in this nucleus decreased the frequency of the single spikes in the medial prefrontal cortex.

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