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The most powerful substance in the human brain for neuronal communication is glutamate. It’s by far the most abundant, and it’s implicated in all kinds of operations.
One of the most amazing is the slow restructuring of neural networks because of memory and learning acquisition, a process called synaptic plasticity. Glutamate is also of deep clinical interest: After stroke or brain injury and in neurodegenerative disease, glutamate can accumulate to toxic levels out of neurons and damage or kill them.
In a paper last fall, Watanabe (along with several MBL Neurobiology course students) described how glutamate is released from neural synapses after the neuron fires. And today, Watanabe printed a followup study in Nature Communications.
With this paper, we uncover how signals are transmitted across synapses to turn on the switch for plasticity. We demonstrate that glutamate is first released near AMPA-type glutamate receptors, to relay the signal from one neuron to the next, and then near NMDA-type receptors immediately after the first signal to activate the switch for synaptic plasticity.”
Shigeki Watanabe, Researcher, School of Medicine, Johns Hopkins University
This new study was also partly conducted in the MBL Neurobiology class, where Watanabe is a faculty member. “It began in 2018 with (course students) Raul Ramos and Hanieh Falahati, and then we followed up in 2019 with Stephen Alexander Lee and Christine Prater. Shuo Li, the first writer, was my teaching assistant for the Neurobiology course for both years,” Watanabe says. He’ll be returning to the MBL this summer to teach in the course — and find more.
Marine Biological Laboratory
Li, S., et al. (2021) Asynchronous release sites align with NMDA receptors in mouse hippocampal synapses. Nature Communications. doi.org/10.1038/s41467-021-21004-x.