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Yihui Cui




u  9/2005 –7/2008

M.S.  Shanghai Institute of Brain Functional Genomics

East China Normal University

Major in Neuroscience (Synaptic plasticity & learning behavior)

u  10/2008-2/2009

1st Pre-PhD rotation Institute of Pasteur Paris

      Project participated: in vivo optical fibre imaging in freely moving mice

u  3/2009-9/2013

2nd Pre-PhD rotation and PhD  Laboratoire de Dynamique et Pathophysiologie des Réseaux Neuronaux

      INSERM U667, Collège de France

      PhD project: Corticostriatal information processing

      Scholarship: L’Ecole des neurosciences paris ile-de-France; France Parkinson

u  10/2013-3/2014

Post-doc Laboratoire de Dynamique et Pathophysiologie des Réseaux Neuronaux

u  8/2017-recent

Post-doc Zhejiang University

u  8/2017-recent

Lecturer Zhejiang University


1.          Astroglial Kir4. 1 in the lateral habenula drives neuronal bursts in depression. Yihui Cui, Yan Yang, Zheyi Ni, Yiyan Dong, Guohong Cai, Alexandre Foncelle, Shuangshuang Ma, Kangning Sang, Siyang Tang, Yuezhou Li, Ying Shen, Hugues Berry, Shengxi Wu, Hailan Hu*. Nature, 2018.

2.          Ketamine blocks bursting in the lateral habenula to rapidly relieve depression. Yan Yang#, Yihui Cui#, Kangning Sang#, Yiyan Dong#, Zheyi Ni, Shuangshuang Ma, Hailan Hu*. Nature, 2018.

3.          Endocannabinoid dynamics gate spike-timing dependent potentiation and depression. Cui Y, Prokin I, Xu H, Delord B, Genet S, Venance L, Berry H. Elife. 2016.

4.          Endocannabinoids mediate bidirectional striatal spike-timing-dependent plasticity. Cui Y, Paillé V, Xu H, Genet S, Delord B, Fino E, Berry H, Venance L. J Physiol. 2015.

5.          Hunting the “black dog” of depression: the functional implication of lateral habenula. Cui Y & Hu H, Chinese Bulletin of life science. 2015.

6.          Endocannabinoids mediate spike-timing dependent potentiation and depression: a model-based experimental approach. Cui Y, Paillé V, Delord B, Genet S, Fino E, Venance L, Berry H. BMC Neuroscience. 2013.

7.          Forebrain NR2B Overexpression Facilitating the Prefrontal Cortex Long-Term Potentiation and Enhancing Working Memory Function in Mice. Cui Y#, Jin J#, Zhang X#, Xu H, Yang L, Du D, Zeng Q, Tsien JZ, Yu H, Cao X. PLoS One. 2011.

8.          Activation of extracellular signal-regulated kinase in the anterior cingulate cortex contributes to the induction of long-term potentiation in rats. Cao H#Cui YH#, Zhao ZQ, Cao XH, Zhang YQ. Neurosci Bull. 2009.

9.          Enhancement of memory function in aged mice by a novel derivative of xanomeline. Cui Y, Wang D, Si W, Lv W, Niu Y, Lei X, Hu Y, Cao X. Cell Res. 2008.

10.      A novel derivative of xanomeline improved memory function in aged mice. Cui YH#, Si W#, Yin L, An SM, Jin J, Deng SN, Cao XH. Neurosci Bull. 2008.

11.      Polymodal activation of the endocannabinoid system in the extended amygdala. Puente N, Cui Y, Lassalle O, Lafourcade M, Georges F, Venance L, Grandes P, Manzoni OJ. Nat Neurosci. 2011.

12.      The effects of NMDA subunit composition on calcium influx and spike timing-dependent plasticity in striatal medium spiny neurons. Evans RC, Morera-Herreras T, Cui Y, Du K, Sheehan T, Kotaleski JH, Venance L, Blackwell KT. PLoS Comput. Bio. 2012.

13.      Distinct coincidence detectors rule the corticostriatal spike timing-dependent plasticity. Fino E, Paillé V, Cui Y, Morera-Herreras T, Deniau JM, Venance L. J physiol. 2010.

14.      Activation of extracellular signal-regulated kinase in the anterior cingulate cortex contributes to the induction and expression of affective pain. Cao H, Gao YJ, Ren WH, Li TT, Duan KZ, Cui YH, Cao XH, Zhao ZQ, Ji RR, Zhang YQ. J Neurosci. 2009.

15. A concurrent excitation and inhibition of dopaminergic subpopulations in response to nicotine. Eddine R, Valverde S, Tolu S, Dautan D, Hay A, Morel C, Cui Y, Lambolez B, Venance L, Marti F, Faure P. Sci Rep2015.


Research work

Hyperactivity of the lateral habenula (LHb) has been reported to be linked with depression status in depressive-like animal models (Li et al., 2011, Li et al., 2013; Shabel et al., 2014). This indicates the firing property of the LHb neurons is changed under stress. In our research, 1) We found with both in vitro and in vivo recordings that LHb neurons display high spontaneous firing and show significantly increased bursting activity in several animal models of depression. Pharmacological experiments and computational modeling revealed that bursting in LHb depends on both hyperpolarization-activated T-type Ca channels (CaVs) and NMDAR activity. Moreover, burst-evoking photostimulation of LHb in vivo causes depressive-like behaviors. Our results demonstrate that LHb burst firing is crucial for depression and that blockade of this burst contributes to the fast antidepressant actions of ketamine. 2) We identified the molecular mechanism responsible for increased LHb bursts in depression. Using high-throughput quantitative proteomic screen, we identified an inward-rectifying potassium channel Kir4.1 to be overexpressed in the LHb of depressed rats. We found that Kir4.1 expression in development correlates with the depresssion onset. Kir4.1 shows distinct expression pattern on the astrocytic membrane processes tightly wrapping around the neuronal cell bodies, supporting its function to buffer extracellular potassium and trigger neuronal hyperpolarization required for burst initiation. Cell-specific overexpression of Kir4.1in LHb astrocytes drives more neuronal bursting and causes depressive symptoms including anhedonia and behavioral despair. Conversely, knocking down Kir4.1or overexpression of its dominant negative form in astrocytes but not neurons reduces bursting and reverses the depressive symptoms. We suggest that the habenular cells, by generating more bursting activity via kir4.1 regulation, in response to a transient change in the activity of the limbic forebrain under depressive status, may contribute to the regulation of the monoaminergic activity in the brain.