Tianyi Mao, Ph.D.
After earning her B.S. in Biological Science and Biotechnology at Tsinghua University in Beijing, China in 1997, Mao received her Ph.D. in Neuroscience from the Johns Hopkins University School of Medicine in 2005. She did postdoctoral research at the Cold Spring Harbor Laboratory and then at the Howard Hughes Medical Institute's Janelia Farm Research Campus. Mao was appointed as an assistant scientist at the Vollum Institute in September 2010.
Summary of Current Research
The basal ganglia are critical for many fundamental brain functions, such as movement control and decision-making. Dysfunction of the basal ganglia contributes to the pathophysiology of many neurodegenerative diseases, most notably Parkinson’s disease and Huntington’s disease. Our understanding of the basal ganglion has been limited by the complexity of the circuitry. For example, increasing evidence suggests that neurons in the basal ganglia are heterogeneous, yet little is known about the anatomical and functional connectivity of individual cell types.
In my laboratory, we examine the functional connectivity within basal ganglia and its interaction with cerebral cortex and thalamus. We target defined cell types by combining novel functional circuit analysis tools and molecular genetic technology with classical anatomical tracing. We also use two-photon imaging with genetically encoded calcium sensors to study the signal transduction events in basal ganglia that underlie the dynamics of functional circuitry.
Alterations in basal ganglia circuits also are associated with behavioral perturbations in drug addiction and neurodegenerative diseases. A mid-term goal of our research program is to investigate how the circuitry changes during different behaviors (e.g. goal-directed vs. habitual), and in animal models of addiction.
These projects are expected to be synergistic. With these complementary approaches, we aim to determine the cell-type specific circuitry, a prerequisite for a mechanistic understanding of basal ganglia function in health and disease.
Hunnicutt BJ, Long BR, Kusefoglu D, Gertz KJ, Zhong H, and Mao T. (2014) A comprehensive thalamocortical projection map at the mesoscopic level. Nature Neurosci. 17:1276-1285.
Hooks BM, Mao T, Gutnisky DA, Yamawaki N, Svoboda K, and Shepherd GM. (2013) Organization of cortical and thalamic input to pyramidal neurons in mouse motor cortex. J. Neurosci. 33:748-760.
Madisen L, Mao T, Koch H, Zhuo JM, Berenyi A, Fujisawa S, Hsu YW, Garcia AJ 3rd, Gu X, Zanella S, Kidney J, Gu H, Mao Y, Hooks BM, Boyden ES, Buzsáki G, Ramirez JM, Jones AR, Svoboda K, Han X, Turner EE, and Zeng H. (2012) A toolbox of Cre-dependent optogenetic transgenic mice for light-induced activation and silencing. Nat. Neurosci. 15:793-802.
Mao T, Kusefoglu D, Hooks BM, Huber D, Petreanu L, and Svoboda K. (2011) Long-range neuronal circuits underlying the interaction between sensory and motor cortex. Neuron 72:111-123.
Lewis TL Jr, Mao T, and Arnold DB. (2011) A role for myosin VI in the localization of axonal proteins. PLoS Biol. 9:e1001021.
Pan WX, Mao T, and Dudman JT. (2010) Inputs to the dorsal striatum of the mouse reflect the parallel circuit architecture of the forebrain. Front. Neuroanat. 4:147.
Tian L, Hires SA, Mao T, Huber D, Chiappe ME, Chalasani SH, Petreanu L, Akerboom J, McKinney SA, Schreiter ER, Bargmann CI, Jayaraman V, Svoboda K, and Looger LL. (2009) Imaging neural activity in worms, flies and mice with improved GCaMP calcium indicators. Nature Methods 12:875-881.
Zhong H, Sia GM, Sato TR, Gray NW, Mao T, Khuchua Z, Huganir RL, and Svoboda K. (2009) Subcellular dynamics of type II PKA in neurons. Neuron 62:363-374.
Lewis TL Jr, Mao T, Svoboda K, and Arnold DB. (2009) Myosin-dependent targeting of transmembrane proteins to neuronal dendrites. Nature Neurosci. 12:568-576.
Petreanu L, Mao T, Sternson SM, and Svoboda K. (2009) The subcellular organization of neocortical excitatory connections. Nature 457:1142-1145.
Mao T, O'Connor DH, Scheuss V, Nakai J, and Svoboda K. (2008) Characterization and subcellular targeting of GCaMP-type genetically-encoded calcium indicators. PLoS One 3:e1796.