Bio

Professional Education


  • Bachelor of Science, National Taiwan University (2003)
  • Master of Science, National Taiwan University (2007)
  • Doctor of Philosophy, University College London (2012)

Stanford Advisors


  • Jun Ding, Postdoctoral Research Mentor

Publications

All Publications


  • Aldehyde dehydrogenase 1a1 mediates a GABA synthesis pathway in midbrain dopaminergic neurons. Science Kim, J., Ganesan, S., Luo, S. X., Wu, Y., Park, E., Huang, E. J., Chen, L., Ding, J. B. 2015; 350 (6256): 102-106

    Abstract

    Midbrain dopamine neurons are an essential component of the basal ganglia circuitry, playing key roles in the control of fine movement and reward. Recently, it has been demonstrated that γ-aminobutyric acid (GABA), the chief inhibitory neurotransmitter, is co-released by dopamine neurons. Here, we show that GABA co-release in dopamine neurons does not use the conventional GABA-synthesizing enzymes, glutamate decarboxylases GAD65 and GAD67. Our experiments reveal an evolutionarily conserved GABA synthesis pathway mediated by aldehyde dehydrogenase 1a1 (ALDH1a1). Moreover, GABA co-release is modulated by ethanol (EtOH) at concentrations seen in blood alcohol after binge drinking, and diminished ALDH1a1 leads to enhanced alcohol consumption and preference. These findings provide insights into the functional role of GABA co-release in midbrain dopamine neurons, which may be essential for reward-based behavior and addiction.

    View details for DOI 10.1126/science.aac4690

    View details for PubMedID 26430123

  • Dynamic rewiring of neural circuits in the motor cortex in mouse models of Parkinson's disease. Nature neuroscience Guo, L., Xiong, H., Kim, J., Wu, Y., Lalchandani, R. R., Cui, Y., Shu, Y., Xu, T., Ding, J. B. 2015; 18 (9): 1299-1309

    Abstract

    Dynamic adaptations in synaptic plasticity are critical for learning new motor skills and maintaining memory throughout life, which rapidly decline with Parkinson's disease (PD). Plasticity in the motor cortex is important for acquisition and maintenance of motor skills, but how the loss of dopamine in PD leads to disrupted structural and functional plasticity in the motor cortex is not well understood. Here we used mouse models of PD and two-photon imaging to show that dopamine depletion resulted in structural changes in the motor cortex. We further discovered that dopamine D1 and D2 receptor signaling selectively and distinctly regulated these aberrant changes in structural and functional plasticity. Our findings suggest that both D1 and D2 receptor signaling regulate motor cortex plasticity, and loss of dopamine results in atypical synaptic adaptations that may contribute to the impairment of motor performance and motor memory observed in PD.

    View details for DOI 10.1038/nn.4082

    View details for PubMedID 26237365

  • Input- and Cell-Type-Specific Endocannabinoid-Dependent LTD in the Striatum CELL REPORTS Wu, Y., Kim, J., Tawfik, V. L., Lalchandani, R. R., Scherrer, G., Ding, J. B. 2015; 10 (1): 75-87

    Abstract

    Changes in basal ganglia plasticity at the corticostriatal and thalamostriatal levels are required for motor learning. Endocannabinoid-dependent long-term depression (eCB-LTD) is known to be a dominant form of synaptic plasticity expressed at these glutamatergic inputs; however, whether eCB-LTD can be induced at all inputs on all striatal neurons is still debatable. Using region-specific Cre mouse lines combined with optogenetic techniques, we directly investigated and distinguished between corticostriatal and thalamostriatal projections. We found that eCB-LTD was successfully induced at corticostriatal synapses, independent of postsynaptic striatal spiny projection neuron (SPN) subtype. Conversely, eCB-LTD was only nominally present at thalamostriatal synapses. This dichotomy was attributable to the minimal expression of cannabinoid type 1 (CB1) receptors on thalamostriatal terminals. Furthermore, coactivation of dopamine receptors on SPNs during LTD induction re-established SPN-subtype-dependent eCB-LTD. Altogether, our findings lay the groundwork for understanding corticostriatal and thalamostriatal synaptic plasticity and for striatal eCB-LTD in motor learning.

    View details for DOI 10.1016/j.celrep.2014.12.005

    View details for Web of Science ID 000347465600008

    View details for PubMedID 25543142

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