澳门官方电子游戏平台

Research Direction


  • Our research is focused on ellucidating neuronal circuitry mechanisms that underlie brain learning and postnatel critical period pleasticity, as well as synaptic pathologies that are associated with neural developmental diseases.

Latest and Featured Publications


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Perinatal exposure to Zika virus causes variable defects in brain funcitons

In this international collaboration study, the teams from China, Brazil and USA have identifed a spectrum of neurodevelopmental abnormalities in both children and mice. Among the findings, we revealed that although mouse brains infected later after birth do not have apparent abnormal brain structure, those mice still show significant impairments of visual cortical functions, circuit organization, and experience-dependent plasticity. Thus, special attention should be paid to all children born to ZIKV infected mothers for screening of abnormal behaviors and sensory function during childhood. See Zhao & Shang et al., (2020) Adv. Sci. [PDF]

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Modeling single-neuron dynamics is the first step to quantitatively understand brain computation. Yet, the existing point neuron models fail to capture dendritic effects. Using realistic neuronal simulations, theoretical analyses, and electrophysiological experiments, we have derived an effective point neuron model, which incorporates an additional synaptic integration current arising from the nonlinear interaction between synaptic currents across spatial dendrites. Their model captures the somatic voltage response of a neuron with complex dendrites and is capable of performing rich dendritic computations. See Li et al., (2019) PNAS. [PDF]

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Autism spectrum disorders (ASDs) include a variety of developmental brain disorders with clinical findings implicating the dysfunction of the left hemisphere. We generate mice lacking one copy of ASD-related genen Sh3rf2 and find that these mice recapture multiple ASD-like behavioral deficits. The Sh3rf2 haploinsufficiency resultes in abnormal excitatory synaptic transmission in the hippocampus, which is remarkably unilateral in the left hemisphere. Thus, our results support a notion that Sh3rf2 haploinsufficiency is a highly penetrant risk factor for ASD. See Wang and Tan et al., (2018) Cell Reports. [PDF]

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Distinct subtypes of inhibitory interneuron are known to shape diverse rhythmic activities in the cortex, but how they interact to orchestrate specific band activity remains largely unknown. In this study, we conducted in vivo recording and manipulating interneuronal spiking activity in the visual cortex of behaving mice and have revealed an explicit neuronal circuitry mechanism by which somatostatin (SOM)- and parvalbumin (PV)-expressing inhibitory interneurons exert differential and cooperative roles in driving cortical beta and gamma oscillations. Our paper was featured in the December issue of Neuron. See Chen et al., (2017) Neuron, 96(6):1403-1418. [PDF+Suppl]

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Entorhinal cortex (EC) transfers multimodal information to hippocampus CA1 neurons via indirect and direct pathways. By using ChR2-assisted circuit mapping method, in vivo optogenetics and electrophysiology, we show that excitatory projections from lateral entorhinal cortex selectively target a subpopulation of morphologically complex, calbindin-expressing pyramidal cells (cPCs) in CA1, forming a distinct direct circuit that is required for olfactory associative learning. The cPCs develop more selective spiking responses to odor cues during learning. See Li et al., (2017) Nat. Neurosci. [PDF] It was a cover story [Cover].

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By systematically examining various intracortical synapses within layer 4 of the mouse visual cortex, demonstrate that in the developing visual cortical circuit, temporal dynamics of intracortical excitatory synapses are selectively regulated by visual experience prior to the critical period onset, while that of intracortical inhibitory synapses and long-range thalamocortical excitatory synapses remained unchanged. This provides an additional essential exciatory circuit mechanism for regulating critical period plasticity. See Miao et al., (2016) Cell Reports [PDF]

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Our study, collaborated with Dr. Le-ping Cheng's group at ION, CAS, showed that expression of single transcriptor factor Ascl1 alone is sufficient to convert astrocytes directly into functional neurons in the intact mouse brain. The transdifferentiated neurons functionally mature progressively and form functional synapses with existing neighboring neurons of various circuits in the postnatal and adult mouse brain. Thus, our work offers potential therapeutic approaches for neural regeneration. See Liu et al. (2015) J. Neurosci., 35(25):9336 鈥9355. [PDF]

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Critical period plasticity describes a developmental process whereby neural circuits are fine-tuned for specific functions. Here, we show that the Rett syndrome protein MeCP2 in GABAergic parvalbumin- expressing neurons is required for maintaining proper inhibitory circuitry functions that underlie the induction of experience-dependent critical period plasticity of the developing visual cortex. The specific locus of cortical synaptic defects caused by MeCP2 loss in inhibitory PV cells was revealed as well. See He et al., (2014) Nat. Commun., 5:5036. [PDF]

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What correlated inputs from the two eyes are responsible for mediating the critical period plasticity in developing V1 remains unclear. Using in vivo whole-cell recording from the mouse V1, we demonstrate that the coincidence of binocular synaptic inputs from the two eyes is a hallmark of the critical period and serves as neural substrates for the induction of experience-dependent ocular dominance plasticity of the developing V1, through a homeostatic synaptic learning mechanism. See Chen et al., (2014) J. Neurosci., 34(8):2940-2955. [PDF]

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Activity-induced synaptic modification provides a cellular basis for developmental refinement of neuronal connections and for the information storage that is associated with learning and memory. Here, we show that at developing hippocamal GABAergic synapses, a bi-directional modification of GABAergic synapses that is induced by repetitive coincident pre- and postsynaptic spiking at different frequenciesand postsynaptic GABA(B)R activation mediates the LTP. See Xu et al., (2008) Nat. Neurosci., 11, 1410 - 1418. [PDF]

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The integretion of synaptic inputs at the dendrite determines the neuronal spike ouput. Based on realistic modeling and experiments in rat hippocampal slices, we derived a simple arithmetic rule for spatial summation of concurrent excitatory glutamatergic inputs (E) and inhibitory GABAergic inputs (I). Our rule offers a simple analytical tool for studying E鈥揑 integration in pyramidal neurons that incorporates the location specificity of GABAergic shunting inhibition. See Hao et al., (2009) PNAS, 106(51) 21906鈥21911. [PDF]