Ponente invitad@: Chaitanya Chintaluri. Metabolic Regulation of Neural Function

What: Metabolic Regulation of Neural Function

Where: BCBL Auditorium and Auditorium zoom room (If you would like to attend to this meeting reserve at info@bcbl.eu)

Who: Chaitanya Chintaluri, Postdoctoral Researcher, Institute of Science and Technology, Austria

When:  Monday,  June 22nd at  12:00 PM/noon

Neurons fire without apparent cause — in sleep, at rest, in isolated slices. Rather than noise, I propose this is a necessity. When ATP consumption falls below a critical threshold, mitochondria accumulate toxic reactive oxygen species (ROS). Since mature neurons maintain no long-term energy reserves, their only rapid recourse is to fire — expending ATP and restoring metabolic equilibrium. I term such firing "metabolic spiking" (Chintaluri & Vogels, PNAS 2023).
In this talk, I will introduce this framework and extend it to synaptic plasticity, arguing that long-term weight changes serve the same homeostatic function on a slower timescale — a single metabolic principle that unifies the diversity of plasticity rules and produces asynchronous networks with stable weights. I will further contextualize epilepsy as hyper-regulation of metabolic spiking, and the loss of such spiking in dopaminergic neurons of the substantia nigra as a candidate driver of Parkinson's disease.
I will close with an outlook on what I believe is an exciting frontier: connecting this metabolic framework to imaging. Because mitochondrial Complex IV is the terminal destination of oxygen in the electron transport chain, the BOLD signal may be understood as a filtered readout of neuronal mitochondrial energy consumption — giving us a roadmap toward deciphering the hemodynamic response from first principles — from mitochondria up. What if the BOLD signal is simply the brain's mitochondria, breathing?