All of our behaviors, thoughts and perceptions stem from the activity of neural circuits: highly precise sets of connections formed between specific types of neurons.
The three major goals of our laboratory are to:
1) Understand the functional architecture of the neural circuits that enable us to see and respond to particular aspects of the visual environment
2) Discover how those circuits achieve specificity of their connections during development
3) Develop strategies to replenish functional visual circuits in response to injury or disease
A cornerstone our work is the identification of genes that are selectively expressed by functionally specialized neurons in the eye and brain. This allows us to delineate the specific circuit connections made by those neurons and to monitor and manipulate their activity during perceptual and behavioral tasks. It also allows us to probe the genes used by those neurons during development to find and form connections with their appropriate synaptic partners.
Extending from these studies of the healthy brain is the exciting opportunity to address whether the mechanisms that assemble functionally precise visual circuits during development can be reactivated in response to diseases that normally cause irreversible blindness, such as glaucoma. To that end, we are using molecular genetic approaches to preserve and re-wire damaged visual circuits, and then testing what sorts of visual perceptions and behaviors those circuits can support.
A genetically identified retinal ganglion cell (RGC) expressing green fluorescent protein. In red are the processes of the interneurons that connect with this RGC and in blue are other RGCs and interneurons. RGCs such as this one connect to the brain and thus are essential for vision.
Osterhout JA, Josten N, Yamada J, Pan F, Wu SW, Nguyen PL, Panagiotakos G, Inoue YU, Egusa SF, Volgyi B, Inoue T, Bloomfield SA, Barres BA, Berson DM, Feldheim DA, Huberman AD (2011) Cadherin-6 Mediates Axon-Target Matching in a Non-Image-Forming Visual Circuit. Neuron 7:632-639.
Koch SM, Dela Cruz CG, Hnasko TS, Edwards RH, Huberman AD, Ullian EM. (2011) Pathway-specific genetic attenuation of glutamate release alters select features of competition-based visual circuit refinement. Neuron 71:235-242
Huberman AD, Niell CM. What can mice tell us about how vision works? (2011) Trends in Neurosciences 34:464-473.
Rivlin-Etzion M, Zhou K, Wei W, Elstrott J, Nguyen PL, Barres BA, Huberman AD, Feller MB (2011) Transgenic mice reveal unexpected diversity of on-off direction selective retinal ganglion cell subtypes and brain structures involved in motion processing. J. Neurosci. 31:8760-8769.
Huberman AD, Clandinin TC, Baier H (2010) Molecular and cellular mechanisms of lamina-specific axon targeting. Cold Spring Harb. Perspect. Biol. 2:a001743.
Huberman AD, Wei W, Elstrott J, Stafford BK, Feller MB, Barres BA (2009) Genetic identification of an On-Off direction selective retinal ganglion cell subtype reveals a layer-specific subcortical map of posterior motion. Neuron 62:327-334.
Huberman AD, Manu M, Koch SM, Susman MW, Brosius Lutz A, Ullian EM, Baccus SA, Barres BA (2008) Architecture and activity-mediated refinement of axonal projections from a mosaic of genetically-identified retinal ganglion cells. Neuron 59:425-438.
Huberman AD, Feller MB, Chapman B (2008) Mechanisms underlying development of visual maps and receptive fields. Annual Revi. Neurosci. 31:479-509.
Huberman AD, Speer CM, Chapman B. (2006) Spontaneous retinal activity mediates development of ocular dominance columns and binocular receptive fields in V1. Neuron 52:247-245.
Huberman AD, Murray KD, Warland DK, Feldheim DA, Chapman B (2005) Ephrin-As mediate targeting of eye-specific projections to the lateral geniculate nucleus. Nature Neurosci., 8:1013-1021.
Huberman AD, Wang GY, Liets LC, Collins OA, Chapman B, Chalupa LM (2003) Eye-specific retinogeniculate segregation independent of normal neuronal activity. Science 300:994-998.
Huberman AD, Stellwagen D, Chapman B (2002) Decoupling eye-specific segregation from lamination in the lateral geniculate nucleus. J. Neurosci. 22:9419-9429.
Andrew Huberman received his Ph.D. in Neuroscience from UC Davis and carried out his postdoctoral training with Dr. Ben Barres in the Department of Neurobiology at Stanford University School of Medicine. Andrew was a Helen Hay Whitney Postdoctoral Fellow and is currently a new faculty member in Biology and Neurosciences at UCSD.