Lab website: www.qiansunlab.org
Our lab studies the function of the hippocampal circuit, a brain area that is vital for memory formation and is linked to many neuropsychiatric disorders, such as PTSD, schizophrenia, and Alzheimer's disease. We use a variety of in vitro and in vivo techniques – including electrophysiology, neuronal tracing, optogenetics and chemogenetics, immunohistochemistry, and mouse behavior – to address the cellular and circuit mechanisms underlying hippocampal information processing and its relevance to behaviors.
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Research Interests
The long term goal of our lab is to help understand the function of the hippocampal circuit, a brain area that is essential for encoding, storage and retrieval of memory and is strongly linked to many neuropsychiatric disorders, such as posttraumatic stress disorder (PTSD), schizophrenia, epilepsy, and Alzheimer's disease.
Current research of our lab is focused on area CA3 in the hippocampus. CA3 is a major component that constitutes the classic trisynaptic circuit in the hippocampus (entorhinal cortex → dentate gyrus → CA3 → CA1), and is crucial for memory storage and pattern completion (a process by which an entire memory is retrieved from degraded or partial cues). Compared to the neighboring CA1 and dentate gyrus, CA3 remains relatively understudied. Our current research aims to address the cellular and circuit mechanisms underlying hippocampal information processing through CA3 circuit. We are also interested in understanding the role of CA3 impairments in neuropsychiatric disorders. Our research contributes to a better understanding of hippocampal circuit function and helps identify novel strategy to relieve or repair behavioral deficits in neuropsychiatric disorders that involve the hippocampus.
Publications
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Selected Publications
Sun Q#, Jiang YQ, Lu MC. (2020) Topographic heterogeneity of intrinsic excitability in mouse hippocampal CA3 pyramidal neurons. J Neurophysiol. 124(4):1270-1284. #corresponding author.
Sun Q#, Buss EW, Jiang YQ, Santoro B, Brann DH, Nicholson DA, Siegelbaum SA#. (2021) Frequency-Dependent Synaptic Dynamics Differentially Tune CA1 and CA2 Pyramidal Neuron Responses to Cortical Input. J Neurosci. 41(39):8103-8110. #co-corresponding author.
Teixeira CM*, Rosen ZB*, Suri P, Sun Q, Hersh M, Sargin D, Dincheva I, Morgan AA, Spivack S, Krok AC, Hirschfeld-Stoler T, Lambe EK, Siegelbaum SA, Ansorge MS. (2018) Hippocampal 5-HT input regulates memory formation and Schaffer collateral excitation. Neuron. 98 (5): 992-1004. *contributed equally.
Sun Q#, Sotayo A, Cazzulino AS, Snyder AM, Denny CA, Siegelbaum SA#. (2017) Proximodistal heterogeneity of hippocampal CA3 pyramidal neuron intrinsic properties, connectivity and reactivation during memory recall. Neuron. 95 (3):656-672. #co-corresponding author.
Srinivas KV, Buss EW, Sun Q, Santoro B, Takahashi H, Nicholson DA, Siegelbaum SA. (2017) The dendrites of CA2 and CA1 pyramidal neurons differentially regulate information flow in the cortico-hippocampal circuit. J Neurosci. 37 (12) 3276-3293.
Sun Q#, Srinivas KV, Sotayo A, Siegelbaum SA#. (2014) Dendritic Na+ spikes enable cortical input to drive action potential output from hippocampal CA2 pyramidal neurons. eLife. 3: doi:10.7554/eLife.04551. #co-corresponding author.
Tatavarty V*, Sun Q*, Turrigiano GG. (2013) How to scale down postsynaptic strength. J Neurosci. 33 (32):13179-13189. *contributed equally.
Sun Q, Turrigiano GG. (2011) PSD-95 and PSD-93 play critical but distinct roles in synaptic scaling up and down. J Neurosci. 31 (18):6800-8.
Ibata K*, Sun Q*, Turrigiano GG. (2008) Rapid synaptic scaling induced by changes in postsynaptic firing. Neuron. 57 (6):819-26. *contributed equally.
Sun Q*, Xing GG*, Tu HY, Han JS, Wan Y. (2005) Inhibition of hyperpolarization-activated current (Ih) suppresses ectopic discharges from injured dorsal root ganglion neurons in a rat model of neuropathic pain. Brain Res. 1032(1-2):63-69. *contributed equally.
Sun Q*, Tu HY*, Xing GG, Han JS, Wan Y. (2005) Ectopic discharges from injured nerve fibers are highly correlated with tactile allodynia only in early, but not late, stage in rats with spinal nerve ligation. Exp Neurol. 191(1):128-136. *contributed equally.