Maria Victoria (MariVi) Tejada-Simon

Learning and Memory

Our research is focused on elucidating the role of the small GTPases in LTP and in hippocampus-dependent learning and memory. In area CA1 of the hippocampus, the most commonly studied form of LTP is dependent on the activation of NMDA receptors. Previously in our laboratory we have found that (1) Rac1 is highly expressed in the adult mouse hippocampus, (2) NMDA receptor activation in hippocampal slices causes Rac1 to translocate to the membrane in a manner similar to that observed in activated phagocytic cells, and (3) translocation of Rac1 interestingly occurs during associative contextual fear learning in the hippocampus of the adult animal. Presently, by using genetically modified animal models, we are investigating whether Rac1 is indeed an important molecule involved post-developmentally in synaptic plasticity in the adult mice, playing a role in the neuro-anatomical and cyto-architectural changes of neurons and in the activation of signal transduction pathways associated with learning and memory processes.

Defective Neuronal Plasticity in Diseases With Cognitive Impairment

A second aspect of our research is the study of diseases with cognitive impairment, such as mental retardation (MR) syndromes, autistic disorders and schizophrenia. Precise synaptic connectivity is essential for normal brain function and the most common neuropathology associated with this type of syndromes is an alteration of this connectivity due to aberrant dendritic spine morphology. Abnormalities in dendrites and spines have been associated with the impaired cognitive abilities, but how they were generated is not yet well understood. It is of great interest to understand the mechanism that lead to lose of synapses and defective synaptic plasticity. In this regard, we have provided evidence pointing to the Rho family of small GTPases, proteins that mediate actin cytoskeleton reorganization, neuronal morphogenesis and gene expression. The role of the small GTPases-linked genes could provide a connection between the mechanism and the neuronal microstructural deficits observed in these cognitive disorders.

Correction of Autistic Traits: A Translational Approach

Our laboratory has reported that animal models of autistic disorders present up-regulation of proteins involved not only in plasticity of neurons but also in the animal’s cognitive behavior. We are studying these proteins as novel therapeutic targets for these human conditions. Using animal models, we are providing insights into the role of these proteins in the autistic brain plasticity and function, as well as exploring new therapeutic possibilities through the pharmacology of novel inhibitors and other traditional treatments.

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