Dan Feldman photo

Dan Feldman

Professor of Neurobiology
Dept of Molecular & Cell Biology
Helen Wills Neuroscience Institute
(510) 643-1723
Research Expertise and Interest
neurobiology, learning, neurophysiology, sensory biology
Research Description

How do neural circuits in the brain’s cerebral cortex mediate sensation, memory, and higher functions, and how does this break down in neurological disease? My lab seeks to answer these questions by studying cortical function at the synaptic, circuit, and information processing levels. We study how cortical circuits process sensory information, adapt to experience, and store information during learning. We investigate the cellular and circuit mechanisms for brain plasticity, and the homeostatic mechanisms that maintain proper cortical function across age and experience. We study the micro-organization of sensory maps in the cortex to reveal principles of information processing and circuit design. We apply this understanding of normal brain function to develop new insights into neurological disorders, including autism.

In the News

In the News

Featured in the Media

Please note: The views and opinions expressed in these articles are those of the authors and do not necessarily reflect the official policy or positions of UC Berkeley.
January 24, 2019
A study using four mouse models is challenging a long-held hypothesis about the brain's activity in autism. The idea has been that neurons in the brain receive too little inhibition or too much excitation in cases of autism, but the new study indicates that the imbalance could be a response mechanism that helps stabilize a brain affected by the disorder. "Many groups are searching for ways to increase inhibition in the brain, either through drugs or through gene therapy, on the assumption that increasing inhibition will restore the brain back to normal," says molecular and cell biology professor Daniel Feldman, a member of the Helen Wills Neuroscience Institute and the study's lead author. "But actually, our results suggest that loss of inhibition might represent a useful compensation that the brain is doing, or might be unrelated to disease symptoms. And if you go in there and increase inhibition, you might make things worse or you might not affect things at all." This story originated at Berkeley News. It has been reprinted in more than a dozen sources.
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