The Wang Lab

Our research goal is to understand how long-term synaptic changes are achieved by the initial neural activation. The activity-dependent neuronal modifications occur at different levels. At the molecular level, signaling molecules, as well as structural molecules, are phosphorylated and de-phosphorylated; certain genes are turned on and off. At the cellular levels, synaptic structures are altered, silent synapses become active, new neurons are born, electrophysiological responses are potentiated or depressed. These changes may ultimately affect our behavior, including learning and memory formation. The abnormality in activity-dependent neuronal responses is also evident in defective brain function associated with neurological diseases. We investigate the linkage between the synaptic molecular events, neurophysiology, and behavioral modifications, as well as the implications leading to therapeutic interventions for certain neurological disorders.

Research Support and Funding:

R01 MH119149 (2019 to 2024), R56 MH118908 (2019 to 2021), R01 MH124992 (2020 to 2024), DoD W81XWH-17-1-0270 (2017 to 2021).

Current research directions in the lab include:

1) mechanisms underlying complexed behavior such as learning and forgetting, stress susceptibility/resilience, and social behavior, 2) mechanisms underlying the pathophysiology of Fragile X syndrome and Bipolar disorder, 3) transcription homeostasis in neurons

Main tools and techniques in the lab:

transgenic mice, primary neuronal and glial cell culture, biochemical and electrophysiology analysis with acute brain slices and live mice, Western blot and immunocytochemistry, transcriptome analysis with RNAseq and RT-PCR, behavioral analysis on learning and memory, locomotion, anxiety, stress responses, and social interaction and social hierarchy.

We have openings for graduate students and postdoctoral research associates. If you are interested, please contact Hongbing Wang (wangho@msu.edu).

Keywords: Adenylyl cyclase (AC), amyloid precursor protein (APP), Alzheimer’s disease (AD), brain derived neurotrophic factor (BDNF), cAMP, cAMP-responsive element (CRE), CREB, extra-cellular regulated protein kinase (ERK), FE65, long-term potentiation (LTP), long-term depression (LTD), memory formation, neuroplasticity, local protein synthesis.