Blakely Lab

The Blakely Lab

The Blakely Lab: Lab Faculty and Postdoctoral Fellows


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Sarah Baas Robinson - Postdoctoral Fellow

Email: sarah.baas@vanderbilt.edu
7150 MRB III

The neurotransmitter dopamine (DA) is a critical modulator of neuronal function in both vertebrate and invertebrates, controlling many behavioral responses, including addiction, motor activity, reward, sleep and arousal. A major control point of DA signaling is the DA transporter (DAT), which limits the magnitude and duration of DA action and is a target of addictive and therapeutic psychostimulants. DAT dysfunction may also contribute to the etiology of DA-linked brain disorders including ADHD, Parkinson’s disease, and schizophrenia. In my project, I capitalize on the powerful forward and reverse genetic approaches available in the model system Caenorhabditis elegans and a novel DA and DAT-dependent behavioral phenotype to evaluate structural determinants of DAT that guide its trafficking to synapses and to identify and characterize regulators of DAT trafficking and function in vivo.





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Nicole Baganz - Postdoctoral Fellow

Email: nicole.baganz@vanderbilt.edu
7144 MRB III

My primary research focus is on receptor and signaling pathways that regulate the expression and activity of the serotonin transporter (SERT). Serotonin (5-hydroxytryptamine, 5-HT) is an important neurotransmitter involved in controlling mood. Alterations in 5-HT neurotransmission are linked to neuropsychological disorders, such as depression. Extracellular levels of 5-HT are tightly controlled by the antidepressant-sensitive SERT. Pro-inflammatory cytokines, released in response to immune challenge and activation of the stress axis, can increase SERT activity and have been shown to generate depressive-like effects on behavior. Using genetic, biochemical, and behavioral approaches, I am using rodent models to investigate the role of IL1R/p38 MAPK signaling pathways in modulating SERT across the lifespan and in relation to autism and mood disorders. Editor's Note: Nicole is also a prolific writer, winning the nonfiction category in the 2011 House Organ writing competition and was the first Guest Writer for Scientific American's The Scicurious Brain Blog.





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Phyllis Freeman-Junior - Visiting Associate Professor

Email: phyllis.freeman@vanderbilt.edu
7140 MRB III

Through the generous support of an NIMH R01 Diversity Supplement, I am pursuing postdoctoral training to acquire sophisticated and contemporary strategies to identify and manipulate genes (or novel connections to DA signaling of known genes) supporting dopamine signaling in C. elegans. My efforts, pursued via a two-year leave from my home institution, Fisk University, will position me to pursue an independent line of research and enhance my mentorship activities in the Fisk-Vanderbilt Masters-to-PhD Bridge Program as well as sponsored undergraduate research initiatives.





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Hideki Iwamoto - Research Assistant Professor

Email: hideki.iwamoto@vanderbilt.edu
7141 MRB III

Presynaptic neurotransmitter transporters play important roles in terminating the transmission and recycling of neurotransmitters. Perturbing neurotransmitter transporters by manipulating genes or administering drugs significantly alters neural activity. In many psychiatric disorders, neurotransmitter transporters can be altered and may contribute to the symptom of these disorders. My research involves the use of electrophysiological methods in combination with fluorescence imaging to assess the functional roles of neurotransmitter transporters on neural activity in brain slice and neuromuscular junction preparations.





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Matt Robson - Postdoctoral Fellow

Email: matthew.j.robson@vanderbilt.edu

7144 MRB III

Serotonin is a crucial neurotransmitter engaged in multiple pathways in the CNS and periphery and is well known to play a key role in the central control of mood, cognition and certain aspects of brain development. Serotonin transporters (SERT) are presynaptic proteins that clear serotonin to aid in cessation of serotonergic signaling, as well as neurotransmitter recycling. Alterations in SERT activity are believed to be involved in the etiology of neuropsychiatric diseases such as depression and autism. Using transgenic animals, behavioral, and biochemical methods, I am working to determine how genetic changes and specific aspects of inflammation effect the regulation of SERT activity within the CNS. In the future, this work may help elucidate new protein and signaling targets for the production of novel pharmacotherapies aimed at treating neuropsychiatric disorders.





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Linda Simmler - Postdoctoral Fellow

Email: linda.simmler@vanderbilt.edu
7148 MRB III

My research focuses on the contributions of serotonin in the acute and chronic actions of cocaine. Cocaine abuse and addiction is a world-wide problem with a significant impact on physical and mental health and overall quality of life. The psychostimulant and rewarding actions of cocaine are well known to relate to the drug's blockade of dopamine transporters. However, cocaine blocks the serotonin and norepinephrine transporters with comparable potency, suggesting that the actions of these neurotransmitters contribute to important aspects of drug action. Using a transgenic mouse model that displays significantly reduced cocaine potency for blockade of the serotonin transporter (SERT Met172), I am elucidating the SERT and serotonin-dependent neuroadaptations that contribute to cocaine action. Hopefully, my research will improve our understanding of the molecular plasticities underlying cocaine action in the brain and lead to better treatments for cocaine addiction.





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Ran Ye - Postdoctoral Fellow

Email: ran.ye@vanderbilt.edu
7144 MRB III

Serotonin transporter (SERT) regulates serotonin levels both in the brain and in the periphery. The expression, function and trafficking of SERT are known to be regulated by a number of SERT-associated proteins, such as PKC, PP2A, Hic-5, and integrin. By using proteomic and biochemical approaches, I am working to identify novel members of the SERT protein complex and understand the mechanism by which SERT is regulated. Through these efforts we also hope the findings can be used to identify serotonin regulatory genes that explain SERT-associated phenotypes associated with genetic variation in mouse and man as well as in mental illness.