VAP spatially stabilizes dendritic mitochondria to locally support synaptic plasticity

Ojasee Bapat, Tejas Purimetla, Sarah Kruessel, Monil Shah, Ruolin Fan, Christina Thum, Fiona Rupprecht, Julian D. Langer and Vidhya Rangaraju ()
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Ojasee Bapat: Max Planck Florida Institute for Neuroscience
Tejas Purimetla: Max Planck Florida Institute for Neuroscience
Sarah Kruessel: Max Planck Institute for Brain Research
Monil Shah: Max Planck Florida Institute for Neuroscience
Ruolin Fan: Max Planck Florida Institute for Neuroscience
Christina Thum: Max Planck Institute for Brain Research
Fiona Rupprecht: Max Planck Institute for Brain Research
Julian D. Langer: Max Planck Institute for Brain Research
Vidhya Rangaraju: Max Planck Florida Institute for Neuroscience

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: Abstract Synapses are pivotal sites of plasticity and memory formation. Consequently, synapses are energy consumption hotspots susceptible to dysfunction when their energy supplies are perturbed. Mitochondria are stabilized near synapses via the cytoskeleton and provide the local energy required for synaptic plasticity. However, the mechanisms that tether and stabilize mitochondria to support synaptic plasticity are unknown. We identified proteins exclusively tethering mitochondria to actin near postsynaptic spines. We find that VAP, the vesicle-associated membrane protein-associated protein implicated in amyotrophic lateral sclerosis, stabilizes mitochondria via actin near the spines. To test if the VAP-dependent stable mitochondrial compartments can locally support synaptic plasticity, we used two-photon glutamate uncaging for spine plasticity induction and investigated the induced and adjacent uninduced spines. We find VAP functions as a spatial stabilizer of mitochondrial compartments for up to ~60 min and as a spatial ruler determining the ~30 μm dendritic segment supported during synaptic plasticity.

Date: 2024
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DOI: 10.1038/s41467-023-44233-8

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