Research: “Peripheral Mechanosensory Neuron Dysfunction Underlies Tactile and Behavioral Deficits in Mouse Models of ASDs”

This study by researchers from Harvard Medical School examined tactile deficits in four groups of mice harboring different genetic mutations, as well as the relationship between tactile deficits, anxiety, and social behavior. The study also focused on the role of the peripheral nervous system and spinal cord in tactile defects. Mice with mutations in the Mecp2, Gabrb3, Shank3, and Fmr1 genes exhibited tactile hypersensitivity in both a texture-specific novel object recognition test and a tactile prepulse (air puff) inhibition assay. Immunohistochemistry was performed on spinal cord sections from Mecp2 mutant mice. The results of this test suggest that lack of inhibition of low-threshold mechanosensory neurons (LTMR) in the spinal cord results in tactile hypersensitivity for Mecp2 mutants. Next, the effects of the Mecp2 and Gabrb3 mutations on anxiety and sociability was measured using an open-field test, a nest building task, a three-chamber social interaction test, and a tube dominance test. The data indicate that tactile defects tramadol hcl resulting from Mecp2 or Gabrb3 deletion during development, but not in adulthood, cause anxiety and social interaction deficits. When Mecp2 was restored in the somatosensory neurons of Mecp-2 null mice, the mice no longer exhibited tactile sensitivity, anxiety-like behavior, or social interaction deficits. Investigating tactile and other sensory impairments further in the future may aid in the development of novel ASD treatments.

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