Robert Malenka
Academic Appointments
- Professor, Psychiatry & Behavioral Science - Psychiatry/Neuroscience/MSLS
- Member, Bio-X
Key Documents
Contact Information
- Academic Offices
Personal Information Email Tel (650) 724-2730
Professional Overview
Administrative Appointments
- Councilor, Society for Neuroscience (2006 - 2010)
- Scientific Advisory Board, Seaside Therapeutics (2007 - 2009)
- Scientific Advisory Board, Pfizer (2008 - 2009)
Honors and Awards
- Medical Research Award in Neuropsychiatry, Robert and Claire Pasarow Foundation (2011)
- Member, National Academy of Sciences (2011)
- Fellow, American Academy of Arts and Sciences (2005)
- Member, Institute of Medicine of the National Academies (2004)
- Associate, Neurosciences Research Program (1999-2006)
- Basic Neuroscience Research Award, Collegium Internationale Neuropsychopharmacologicum-Lilly (2002)
Postdoctoral Advisees
Gul Dolen, Marc Fuccillo, Debanjan Goswami, Scott Hayton, Lin Hung, Byungkook Lim, Jai Polepalli, Neil Schwartz, Paul Temkin, Di Wu
Graduate & Fellowship Program Affiliations
Industry Relationships
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Scientific Focus
Current Research Interests
Long-lasting activity-dependent changes in the efficacy of synaptic transmission play an important role in the development of neural circuits and may mediate many forms of learning and memory. Work from my laboratory over the last 10 years has demonstrated that there are a variety of related but mechanistically distinct forms of synaptic plasticity. A major goal of my laboratory is to elucidate both the specific molecular events that are responsible for the triggering of these various forms of synaptic plasticity and the exact modifications in synaptic proteins that are responsible for the observed, long-lasting changes in synaptic efficacy. To accomplish this we use cellular electrophysiological recording techniques to examine synaptic plasticity in a variety of different in vitro preparations including thin slices of various regions of the rodent brain and primary neurons in culture. We also use cell biological and molecular techniques to examine the activity-dependent modulation of neurotransmitter receptors and to express dominant negative forms of various synaptic proteins so that their exact functions can be determined. An additional complementary approach has involved examining synaptic physiology and synaptic plasticity in various mutant mouse lines lacking specific synaptic proteins.
A related but independent area of research in my laboratory is the elucidation of the synaptic action of drugs of abuse such as the psychostimulants cocaine and amphetamine. Toward this end, we have developed in vitro slice preparations of the nucleus accumbens and ventral tegmental area, brain regions which are thought to mediate several of the behavioral effects of drugs of abuse. We have characterized a novel form of synaptic plasticity in the nucleus accumbens and have done an extensive pharmacological characterization of the synaptic effects of dopamine, cocaine, and amphetamine. Currently we are examining in more detail the underlying mechanisms of dopamine's actions and determining how chronic treatment with drugs of abuse affect the synaptic responses of nucleus accumbens and ventral tegmental area cells. Because chronic exposure to drugs of abuse elicit long-term adaptive changes in critical neural circuits, it is hoped that the knowledge gained from the work on the molecular mechanisms underlying synaptic plasticity will provide important clues to the molecular mechanisms underlying the development of tolerance, dependence and addiction.
Publications
- Diverging neural pathways assemble a behavioural state from separable features in anxiety. Nature. 2013; (7444): 219-23
- LTP requires a unique postsynaptic SNARE fusion machinery. Neuron. 2013; (3): 542-58
- Anhedonia requires MC4R-mediated synaptic adaptations in nucleus accumbens. Nature. 2012; (7406): 183-9
- Comprehensive qPCR profiling of gene expression in single neuronal cells. Nat Protoc. 2012; (1): 118-27
- Distinct neuronal coding schemes in memory revealed by selective erasure of fast synchronous synaptic transmission. Neuron. 2012; (5): 990-1001
- Input-specific control of reward and aversion in the ventral tegmental area. Nature. 2012; (7423): 212-7
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