Presenter Information

Tyler Felton, University of Wyoming

First Advisor

Dr. Qian-Quan Sun

Description

This study focused on the cytoarchitectonic and immunohistological differences in GABA-releasing and Glutamate-releasing interneurons between Fmr1 knock-out (FMR1KO) and wild-type (WT) mice in the posterior piriform cortex. Our results showed a robust reorganization of the neocortical inhibitory and excitatory circuits in the FMR1KO mouse. The reorganization is characterized by a significant reduction (15%, p<0.001) in the densities of GAD-67-postive cells, while a significant increase of both GluR1 (9%, p<0.001) and GluR2 (20%, p<0.001) AMPA receptor subunits was also observed. Additionally, there was a modest but significant increase in the layer 2 total cell density in the FMR1KO mouse. These results provide the first report showing significant alterations of both GABA-releasing and Glutamate-releasing interneurons in the posterior piriform cortex in the mouse model of fragile X syndrome. Uncovering the changes in specific GABAergic and Glutamatergic circuits could help elucidate the mechanisms underlying behavior deficits of fragile X syndrome and autism.

Comments

Oral Presentation, Wyoming NSF EPSCoR

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Cytoarchitectonic and Immunohistological Profile of GABAergic and Glutamatergic Neurons in the Posterior Piriform Cortex in Fragile X Mice

This study focused on the cytoarchitectonic and immunohistological differences in GABA-releasing and Glutamate-releasing interneurons between Fmr1 knock-out (FMR1KO) and wild-type (WT) mice in the posterior piriform cortex. Our results showed a robust reorganization of the neocortical inhibitory and excitatory circuits in the FMR1KO mouse. The reorganization is characterized by a significant reduction (15%, p<0.001) in the densities of GAD-67-postive cells, while a significant increase of both GluR1 (9%, p<0.001) and GluR2 (20%, p<0.001) AMPA receptor subunits was also observed. Additionally, there was a modest but significant increase in the layer 2 total cell density in the FMR1KO mouse. These results provide the first report showing significant alterations of both GABA-releasing and Glutamate-releasing interneurons in the posterior piriform cortex in the mouse model of fragile X syndrome. Uncovering the changes in specific GABAergic and Glutamatergic circuits could help elucidate the mechanisms underlying behavior deficits of fragile X syndrome and autism.