Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at 
a Mammalian Central Synapse

Montesinos, Mónica S.; Dong, Wei; Goff, Kevin; Das, Brati; Guerrero-Given, Debbie; Schmalzigaug, Robert; Premont, Richard T.; Satterfield, Rachel; Kamasawa, Naomi; Young, Samuel M., Jr.

doi:10.1016/j.neuron.2015.10.042

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Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse

MPS-Authors

Montesinos, Mónica S.
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Dong, Wei
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Goff, Kevin
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Das, Brati
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Guerrero-Given, Debbie
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Satterfield, Rachel
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Kamasawa, Naomi
Max Planck Florida Institute for Neuroscience, Max Planck Society;

Young, Samuel M., Jr.
Max Planck Florida Institute for Neuroscience, Max Planck Society;

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http://dx.doi.org/10.1016/j.neuron.2015.10.042
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Citation

Montesinos, M., Dong, W., Goff, K., Das, B., Guerrero-Given, D., Schmalzigaug, R., et al. (2015). Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse. Neuron, 88(5), 918-925. doi:10.1016/j.neuron.2015.10.042.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0029-C7A5-9

Abstract

A cytomatrix of proteins at the presynaptic active zone (CAZ) controls the strength and speed of neurotransmitter release at synapses in response to action potentials. However, the functional role of many CAZ proteins and their respective isoforms remains unresolved. Here, we demonstrate that presynaptic deletion of the two G protein-coupled receptor kinase-interacting proteins (GITs), GIT1 and GIT2, at the mouse calyx of Held leads to a large increase in AP-evoked release with no change in the readily releasable pool size. Selective presynaptic GIT1 ablation identified a GIT1-specific role in regulating release probability that was largely responsible for increased synaptic strength. Increased synaptic strength was not due to changes in voltage-gated calcium channel currents or activation kinetics. Quantitative electron microscopy revealed unaltered ultrastructural parameters. Thus, our data uncover distinct roles for GIT1 and GIT2 in regulating neurotransmitter release strength, with GIT1 as a specific regulator of presynaptic release probability.