Hugo Tejeda, Ph.D.
Unit on Neuromodulation and Synaptic Integration
Dr. Tejeda completed his Ph.D. in Neuroscience at the University of Maryland School of Medicine and at the National Institute on Drug Abuse under the mentorship of Drs. Patricio O’Donnell and Toni Shippenberg. His thesis work elucidated the role of neuromodulatory systems, including opioid receptors, in modulating synaptic integration in prefrontal cortical and limbic circuits. He completed a post-doctoral fellowship in the laboratory of Dr. Antonello Bonci at the National Institute Drug Abuse where he elucidated the mechanisms by which monoamine and opioid receptors, as well as stress modulate information processing in the nucleus accumbens. Dr. Tejeda joined the National Institute of Mental Health in 2018 as a Stadtman principal investigator. His research focuses on the role of neuromodulation in processing information in limbic neural circuits under physiological conditions and in psychiatric disorders.
Research in Dr. Tejeda’s laboratory is aimed at elucidating how the brain utilizes neuromodulation in motivational and emotional neural circuits to process information and orchestrate behavior. Another major focus of the laboratory is to identify plastic changes in neuromodulation and synaptic integration in limbic circuits of animal models of psychiatric disorders to elucidate novel therapeutic targets and increase our understanding of conventional therapies. The laboratory employs an inter-disciplinary approach including electrophysiological, in-vivo imaging, optogenetic, and viral and transgenic techniques to dissect the function of neuromodulators, such as opioid receptors, in regulating synaptic integration in single cells, microcircuits, and distributed limbic networks to control motivated behavior.
Pignatelli* M, Tejeda* HA, Barker DJ, Bontempi L, Wu J, Lopez A, Palma Ribeiro S, Lucantonio F, Parise EM, Torres-Berrio A, Alvarez-Bagnarol Y, Marino RAM, Cai ZL, Xue M, Morales M, Tamminga CA, Nestler EJ, Bonci A (2020) Cooperative synaptic and intrinsic plasticity in a disynaptic limbic circuit drive stress-induced anhedonia and passive coping in mice. Mol Psychiatry, in press (e-pub ahead of print) https://doi.org/10.1038/s41380-020-0686-8*Equalcontribution;co-correspondingauthors. [Pubmed Link]
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