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I received my Ph.D. in Biology during December of 2006 under the supervision of Dr. Sandra Peña de Ortiz. My dissertation work was focused on characterizing genes regulated by the cAMP response element binding protein (CREB) in fear memory consolidation. Since my beginning in research I have always been interested and fascinated in understanding the mechanisms used by the central nervous system to acquire, process, and store information.
I had the opportunity to work on a project in collaboration with Dr. Alcino Silva at the University of California, Los Angeles (UCLA) focused on the molecular characterization of cAMP response element binding protein (CREB) in emotional learning and memory. The research involved the use of a tamoxifen-inducible transgenic CREB repressor system (CREBIR) in mice for contextual fear conditioning and the establishment of a CREB-dependent gene expression profile using a cDNA microarray approach.
Specifically I was validating by Northern blots some of the candidate genes regulated by CREB in contextual fear conditioning, that I identified with cDNA microarray studies previously mentioned. Among those genes was 14-3-3eta, a gene that has been associated with schizophrenia. The microarray studies and the Northern blot of 14-3-3eta, confirming its induction and regulation by CREB in the whole brain after contextual fear conditioning were published on Nature Neuroscience in a work title “CREB required for the stability of new and reactivated fear memories” (Kida et al. 2002).
As a consequence of the results from the published cDNA microarray studies and the fact that I had the CREBIR mice available in the lab, I became interested in studying the possible role of 14-3-3eta in emotional memory. The 14-3-3eta gene encodes a member of a family of signaling proteins, highly abundant in the brain neurons that modulate the function of other proteins via mechanisms involving protein-protein interaction. 14-3-3eta contains a cAMP Responsive Elements (CREs) in its upstream promoter region and is a potential novel learning and memory gene, which may be important in cellular processes downstream of CREB activation that are important for memory consolidation.
As part of my dissertation research I worked on the regional and temporal characterization of 14-3-3eta expression in wild type mice during contextual fear conditioning by In situ hybridization, and Western blot analysis. An additional aim of my dissertation work was to further characterize 14-3-3eta hippocampal CREB-dependent regulation in context fear conditioning using the CREBIR transgenic mice by Immunohistochemistry analysis.
In the summer of 2005 I was selected to participate of the “Advance Techniques in Molecular Neuroscience Course” offered at Cold Spring Harbor Laboratory, NY and instructed by Dr. James Eberwine, Dr. Cary Lai, and Dr. Thomas Hughes.
While working on my dissertation project I developed an interest in neurodevelopmental processes, dynamic mechanisms of synapse formation, and cognition. Particularly, I decided that for my future postdoctoral research experience I want to work on the characterization of mechanisms by which a particular population of mRNAs is transported to synapses and locally translated to modulate synaptic plasticity in the brain, and how these processes relates to learning and memory formation.
In January 2007, I joined Dr. Eric Klann’s laboratory as a postdoctoral fellow at the Center for Neural Science, New York University (NYU). Dr. Klann’s laboratory research focused on the molecular mechanisms involved in synaptic plasticity events such as hippocampal long-term potentiation (LTP) and long-term depression (LTD) and understanding how these mechanisms might relate to learning and memory formation in the brain.
Particularly, one of Dr. Klann’s laboratory areas of interest is the characterization of NMDA and metabotropic glutamate receptors signaling cascade that participate in regulating protein translation initiation factors during LTP, LTD, and hippocampal-dependent memory. Furthermore, in Klann’s laboratory the approach of using genetically-modified mice allows to better understanding the molecular mechanisms required to maintain long-term synaptic plasticity in the brain, and to create animal models for studying neurological diseases characterized by memory impairment and mental retardation.
My work consists of the characterization of TSC-2 transgenic mice during events of hippocampal plastcity (L-LTP and mGluR LTD) and memory, as well as during social behavior paradigms. TSC-2, also known as tuberin, is part of the mTOR signaling pathway which is involved in regulating the initiation of protein synthesis in response to neuronal stimulation. These TSC-2 transgenic mice are a model to study autism, mental retardation, as well as epilepsy.
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