Research Interests

1) Using optogenetics,behavioral assays and electrophysiological methods to explore innate fear related neural circuitry in brain.

2) Functional significance and molecular, cellular mechanism for experience dependent plasticity ofthalamic relay synapses.

3) Role of astrocytes in synapse elimination and long-term memory.

4) Test the role of corresponding pathogenic genes (such as Mecp2, Frm1) in the development of neural circuits.

Research methods

1) Whole cell patch recording in acute brain slices;

2) in vivo extracellular electrophysiological recording in free moving mice;

3) Animal behavioral assays, such as Water maze and T-maze;

4) PCR and Western-blotting and other molecular methods;

5) Optogenetics combine with functional brain imaging;

6) Retrograde or antegrade virus tracking.

Neural circuitry for innate fear

Innate fear is a kind of inherited fear of specific objects, environment or situation without learning. For example, rodents are fear of cats by nature. Even native mice will express fear response in the present of a cat. This emotion trigged by a perceived threat usually causes a quick response, such as freezing, flee or hide, and thus has a profound role for survival and health for all species. Abnormal innate fear in humans particularly phobias and panic disorders is highly associated with anxiety disorder. Recent studies suggested that innate fear induced by different cues were attributed by distinctive neural circuits. Vision and auditory cues, but not olfactory cue induced innate fear is related amygdala. So far, which parts of the brain are involved in olfactory cue induced innate fear remains unclear. We will combine electrophysiological, immunohistochemical, optogenetics and animal behavioral assays to explore the neural circuit for odor induced innate fear.

Mechanisms of synapse elimination

Synapse elimination, selectively removing of unwanted synapses while strengthening wanted synapse, is a key mechanism in the formation of functional neural circuit. During early development, there're redundant synaptic connections in the brain. Most of the synapses will be eliminated in an activity dependent manner during development. If this process was disrupted by either genetic mutations or environmental changes, it will lead to some neurological diseases including autism and schizophrenia. Our early work has established a model in mouse thalamic sensory synapses to study synapse elimination. Now we will explore the mechanism of synapse elimination (particularly role of astrocytes), and role of sensory experience by using of transgenetic mice, electrophysiological recording and immunohistochemistry.

We have postdoc associate position available