BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Memento EPFL//
BEGIN:VEVENT
SUMMARY:BMI Special Seminar // Pierre J. Magistretti: Neuron-glia metaboli
 c coupling: relevance for neuroenergetics\, plasticity and neuropsychiatri
 c diseases
DTSTART:20261119T161500
DTEND:20261119T171500
DTSTAMP:20261110T014600Z
UID:6c460aec6a39fb8225e1a7414130dcc5c57a583634548cb0086b553f
CATEGORIES:Conferences - Seminars
DESCRIPTION:Pierre J. Magistretti\, Division of Biomedical Sciences\, KAU
 ST\, Thuwal\, Saudi Arabia\nA tight metabolic coupling between astrocytes 
 and neurons is a central feature of brain energy metabolism (Magistretti a
 nd Allaman\, Neuron 2015\; Nat Rev Neurosci 2018\; Bolaños and Magistrett
 i\, Nat Metab 2025). Over the years\, my lab has identified and molecularl
 y characterized two key mechanisms of neurometabolic coupling: neuromodula
 tor (VIP\, adenosine\, and noradrenaline)-induced glycogenolysis in astroc
 ytes (Magistretti et al.\, PNAS 1981\; Magistretti et al.\, J. Neurosci 19
 86) and glutamate-stimulated aerobic glycolysis (Pellerin and Magistretti\
 , PNAS 1994). Both processes lead to the release of lactate from astrocyte
 s\, which serves as an energy substrate for neurons as defined by the Astr
 ocyte-Neuron Lactate Shuttle (ANLS) model.\n\nSubsequent work in my lab sh
 owed that lactate also acts as a signaling molecule\, enhancing NMDA recep
 tor activity\, promoting long-term memory\, and activating gene expression
  programs linked to synaptic plasticity (Suzuki et al.\, Cell 2011\; Yang 
 et al.\, PNAS 2014\; Margineanu et al.\, Front Neurosci 2018\; Vezzoli et 
 al.\, Cereb Cortex 2019). Electrophysiological and behavioral studies furt
 her demonstrated that astrocytic lactate supply is activity-dependent and 
 scales with computational demand (Dembitskaya et al.\, PNAS 2022). Recent 
 data indicate that lactate potentiates NMDAR currents via monocarboxylate 
 transporter (MCT)-dependent neuronal uptake\, conversion to pyruvate\, inc
 reased NADH\, and redox-sensitive modulation of GluN2B subunits\, involvin
 g CaMKII signaling (Fiumelli et al.\, J Physiol\, 2026).\n\nRecent preclin
 ical studies in conditions in which pharmacological stimulation of the ANL
 S restores behavioral deficits present in hypometabolic conditions such as
  Glut1 deficiency syndrome (de Vivo disease) and Alzheimer’s disease sup
 port the strategy of targeting astrocytes to overcome brain hypometabolism
  (Beard et al.\, Front Physiol 2022\; Lengacher et al.\, Pharmaceuticals 2
 026). In preclinical models of depression\, lactate was shown to exert ant
 idepressant effects that depend on neurogenesis (Carrard et al.\, Mol Psyc
 hiatry 2018\, 2021).\n\nTogether\, these findings establish lactate as a m
 etabolic–signaling nexus linking astrocyte function to neuronal computat
 ion\, plasticity\, and behavior\, and open new therapeutic perspectives fo
 r neurodegenerative\, mood\, and metabolic brain disorders.\n 
LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717 https://epfl.zoom.u
 s/j/64813563657
STATUS:CONFIRMED
END:VEVENT
END:VCALENDAR