Kelsey C. Martin, M.D., Ph.D.


Dean, David Geffen School of Medicine at UCLA

Professor, Biological Chemistry

Psychiatry and Biobehavioral Sciences

Awards and Honors:

Columbia University, New York Neurobiology

Society for Neuroscience Presidential Lecturer

FASEB/EMBO Chair, Meeting on RNA Localization

Gordon Research Conference Chair, Meeting on Cell Biology of the Neuron

UCLA Postdoctoral Fellow Mentorship Award

FASEB/EMBO Chair, Meeting on RNA Localization

NARSAD Distinguished Investigator Award

H.G. Magoun Lecture Brain Research Institute, UCLA

Dean's Recognition Award

NARSAD Independent Investigator Award

UCLA Eleanor Leslie Term Chair in Innovative Brain Research

EJLB Foundation Scholar Award

American Society of Neurochemistry Jordi Folch-Pi Award

Klingenstein Fellowship in the Neurosciences

McKnight Scholar Award

W.M. Keck Foundation Distinguished Young Scholar Award

NARSAD Daniel X. Freeman Award

Burroughs Wellcome Fund Career Award in the BiomedicalSciences

NARSAD Young Investigator Award

Contact Information

Lab Number: (310) 794-9502
Office Phone Number: (310)794-9507

Office Address:

UCLA Biol Chem
615 Charles E Young
BOX 951737, 390-B BSRB
Los Angeles, CA 90095

Work Address:

615 Charles E. Young Dr. S.
Los Angeles, CA 90095


How Does the Brain Store Memories?

Experience changes the strength and number of synaptic connections between neurons in the brain. This process, known as synaptic plasticity, provides a cellular mechanism for memory storage. Research in the Martin lab is aimed at understanding the cell and molecular biology of synaptic plasticity in mouse and Aplysia model systems. The results of their research shed light not only on healthy brain function, but also on the causes of many brain disorders in which neuronal plasticity and memory formation are altered, including mental retardation, autism spectrum disorders, drug addiction, anxiety disorders, and Alzheimer’s disease.

Long-term forms of plasticity, such as those underlying long-term memory, require new RNA and protein synthesis. This means that signals are transported from the synapse, where they are generated, to the nucleus, where they alter transcription. The transport of molecules from the synapse to the nucleus of neurons is particularly challenging because synapses are often very far from the cell body. The Martin lab has discovered a role for the active transport of signals from stimulated synapses to the nucleus during long-term neuronal plasticity. Current research is aimed at identifying synaptically localized signaling molecules that undergo stimulus-induced active nuclear import during plasticity, and at understanding the cell biological pathways that mediate long-distance retrograde transport from synapse to nucleus. In studies focused on the transcriptional regulator CRTC1, the Martin lab is exploring how specific patterns of neuronal stimulation trigger specific programs of transcription, and how neuromodulators such as dopamine and norepinephrine regulate the programs of gene expression that give rise to long-lasting plasticity. This work provides molecular insights into the role of emotion and attention in memory formation.

Research in the Martin lab also addresses the mechanisms by which transcription-dependent plasticity can occur at subsets of the thousands of synapses that are made by an individual neuron. Dr. Martin and her colleagues have shown that one important mechanism for restricting gene expression to stimulated synapses involves the regulated translation of synaptically localized mRNAs. Studies in her lab are aimed at identifying the populations of mRNAs that localize to synapses, the molecular mechanisms underlying the localization and translation of these mRNAs, as well as the function of local translation in long-term memory. Recent transcriptome and translatome profiling experiments suggest that the regulation of gene expression in neurons is highly decentralized and compartmentalized during plasticity, with transcriptional regulation placing the entire neuronal arbor in a state of readiness to respond to local cues via local translation to change the structure and function of subsets of synapses.