We use a variety of techniques including electrophysiology, immunocytochemisty, imaging, optogenetics, tissue culture, molecular biology and in vivo physiology and animal models to study the functional changes of the central nervous system in physiological and pathological conditions. Our current research interests include:
- Modulation of synaptic transmission and plasticity in the hippocampus and entorhinal cortex. Using infrared video microscopy and patch-clamp recording techniques, we are able to record the synaptic activity or ion channel currents from visually identified neurons in slices. The synaptic activities and ion channel functions are modulated by numerous modulators including neurotransmitters and neuropeptides. We are exploring the underlying cellular and molecular mechanisms using molecular biology, pharmacology and transgenic animal models.
- The functional changes of neurons induced by the neurotransmitters and neuromodulators are likely to be responsible for a variety of physiological functions such as learning and memory or clinical disorders including epilepsy, anxiety, Alzheimer's disease, schizophrenia and autism. We are using in vivo disease models to study the roles of these neuromodulators in these clinical disorders. Our research would likely to provide clues at the molecular and cellular levels to treat neurological diseases.
Selected Publications:
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Boyle CA, Kola PK, Oraegbuna CS, Lei S. Leptin excites basolateral amygdala principal neurons and reduces food intake by LepRb-JAK2-PI3K-dependent depression of GIRK channels. J Cell Physiol. 2024 239:e31117
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Boyle CA, Lei S. Neuromedin B excites central lateral amygdala neurons and reduces cardiovascular output and fear-potentiated startle. J Cell Physiol. 2023, 238:1381-1404.
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Boyle CA, Hu B, Quaintance KL, Mastrud MR, Lei S. Ionic signalling mechanisms involved in neurokinin-3 receptor-mediated augmentation of fear-potentiated startle response in the basolateral amygdala. J Physiol. 2022, 600:4325-4345.
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Lei S, Boyle CA, Mastrud M. PLCβ-Mediated Depletion of PIP2 and ATP-Sensitive K+ Channels Are Involved in Arginine Vasopressin-Induced Facilitation of Neuronal Excitability and LTP in the Dentate Gyrus. eNeuro. 2022 9(4):ENEURO.0120-22.2022.
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Hu B, Boyle CA, Lei S. Roles of PLCβ, PIP2 , and GIRK channels in arginine vasopressin-elicited excitation of CA1 pyramidal neurons. J Cell Physiol. 2022, 237:660-674.
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Lei S, Hu B.Ionic and signaling mechanisms involved in neurotensin-mediated excitation of central amygdala neurons. Neuropharmacology. 2021, 196:108714.
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Lei S, Hu B, Rezagholizadeh N. Activation of V1a vasopressin receptors excite subicular pyramidal neurons by activating TRPV1 and depressing GIRK channels. Neuropharmacology. 2021, 190:108565.
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Boyle CA, Hu B, Quaintance KL, Lei S. Involvement of TRPC5 channels, inwardly rectifying K+ channels, PLCβ and PIP2 in vasopressin-mediated excitation of medial central amygdala neurons. J Physiol. 2021, 599:3101-3119.
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Hu B, Boyle CA, Lei S. Activation of Oxytocin Receptors Excites Subicular Neurons by Multiple Signaling and Ionic Mechanisms. Cereb Cortex. 2021, 31:2402-2415.
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Hu B, Boyle CA, Lei S. Oxytocin receptors excite lateral nucleus of central amygdala by phospholipase Cβ- and protein kinase C-dependent depression of inwardly rectifying K+ channels. J Physiol. 2020, 598:3501-3520.
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Li H, Hu B, Zhang HP, Boyle CA, Lei S. Roles of K+ and cation channels in ORL-1 receptor-mediated depression of neuronal excitability and epileptic activities in the medial entorhinal cortex. Neuropharmacology. 2019, 151:144-158.
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Xiao Z, Cilz NI, Kurada L, Hu B, Yang C, Wada E, Combs CK, Porter JE, Lesage F, Lei S. Activation of neurotensin receptor 1 facilitates neuronal excitability and spatial learning and memory in the entorhinal cortex: beneficial actions in an Alzheimer's disease model. Journal of Neuroscience 2014, 34:7027-7042.
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Deng PY, Xiao Z, Jha A, Ramonet D, Matsui T, Leitges M, Shin HS, Porter JE, Geiger JD, Lei S. Cholecystokinin Facilitates Glutamate Release by Increasing the Number of Readily Releasable Vesicles and Releasing Probability. Journal of Neuroscience. 2010 30:5136-5148
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Deng PY, Xiao Z, Yang C, Rojanathammanee L, Grisanti L, Watt J, Geiger JD, Liu R, Porter JE, Lei S. GABAB receptor activation inhibits neuronal excitability and spatial learning in the entorhinal cortex by activating TREK-2 K+ channels. Neuron 2009, 63:230-243.
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Xiao Z, Deng PY, Rojanathammanee L, Yang C, Grisanti L, Permpoonputtana K, Weinshenker D, Doze VA, Porter JE and Lei S. Noradrenergic depression of neuronal excitability in the entorhinal cortex via activation of TREK-2 K+ channels. Journal of Biological Chemistry. 2009, 284: 10980-10991
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Deng PY, Porter JE, Shin HS, Lei S. Thyrotropin-releasing hormone increases GABA release in rat hippocampus. Journal of Physiology. 2006, 577:497-511.
Dr. Lei's Biography
https://www.ncbi.nlm.nih.gov/myncbi/saobo.lei.1/bibliography/public/
- Postdoctoral training, University of Toronto, National Institutes of Health
- PhD Pharmacology, University of Alberta
- MS Pharmacology, Sun Yat-sen University
- MD Medicine, Sun Yat-sen University