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Sponsored by: Neuroscience Institute
Seminars: SPiNES Seminar - "Powering the Synapse on Demand"
Start Date/Time: 6/14/2018 12:00 PM
End Date/Time: 6/14/2018 1:00 PM
Location: Science Building, Seminar Room SB 103
Description: Cognitive function is an energy-consuming process that requires precise regulation of ATP production to ensure energetic homeostasis and proper synaptic transmission. However, it has not been clear what mechanisms account for activity-driven upregulation of presynaptic ATP production via glycolysis and oxidative phosphorylation. I will present a feedback pathway for upregulation of glycolysis in response to neuronal activity that is essential for metabolic support of synaptic function. During action potential firing, consumption of ATP activates the energy sensor AMPK to drive the insertion of the glucose transporter GLUT4 to presynaptic endings, thereby increasing glucose uptake and its glycolytic conversion to ATP. This metabolic module has important implications for brain function, and may explain why neuronal activity declines rapidly during ischemic attacks and acute hypoglycemia. ATP production through mitochondrial oxidative phosphorylation is similarly upregulated in firing synapses. We have uncovered a feedforward pathway in which mitochondrial Ca2+ uptake via the MCU complex stimulates ATP synthesis and supports synaptic function. Due to the unique structural composition of their MCU complex, neuronal mitochondria take up Ca2+ more readily than other cell types allowing them to fine-tune mitochondrial ATP production to the energetic demands of synaptic activity. This work lays the foundation for understanding how dysregulation of neuronal energetics may lead to cognitive impairments that occur in metabolic diseases such as diabetes.
Contact: Rihan Hassad
Phone: 3-9474
Email: Rihan.Hassad@nyumc.org
Speaker: Ghazaleh Ashrafi, PhD
Speaker Institution: Weill Cornell (Ryan Lab)
Speaker Position: Postdoc
Seminar Host: Rachel Redler (Burden Lab)
Refreshments: No
Fee Required: No
Fee Amount:
 

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