Synaptic Connectivity in Fragile-X Syndrome

Please write research paper on following, also refer to attached articles and no plagiarism/ please avoid repetitive sentences: Fragile X Syndrome is the most common known genetic cause of autism. Fmr1-KO mouse, lacks the Fragile X Mental Retardation Protein (FMRP), and is used as a model of the syndrome. This protein aids in the synthesis of mRNA by stabilizing it, therefore, certain proteins aren’t produced properly which is linked to improper synaptic connectivity in relation to the hippocampus (for memory, plasticity) and cerebellum (balance, movement coordination). The core behavioral deficits of autism may be conceptualized either as excessive adherence to patterns as seen in repetitive actions and aberrant language, or as insensitivity to subtle but socially important changes in patterns. The hippocampus receives information from the entorhinal cortex and plays a crucial role in the processing of patterned information. The function of the hippocampus is pattern completion from entering separated information, forming episodic memories. In this study, we used paired-pulse stimulation of the afferent perforant path and recorded from the CA3 region of the hippocampus. We further identify how active synaptic events occur in the hippocampus by using confocal microscope and green fluorescent protein (labels mGluR5), and blue fluorescent protein (labels NMDA). Also include how lack of the FMRP affects the granule cell layer, transitional zone, and molecular layer in the hippocampus. As for the cerebellum, include how Purkinje cells, climbing fibers, and dendritic cells are affected by lack of FMRP as well.