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Related Experiment Video

Updated: Oct 30, 2025

Presynaptically Silent Synapses Studied with Light Microscopy

Presynaptically Silent Synapses Studied with Light Microscopy

Published on: January 4, 2010

ATR regulates neuronal activity by modulating presynaptic firing.

Murat Kirtay¹, Josefine Sell², Christian Marx¹

¹Leibniz Institute on Aging - Fritz Lipmann Institute (FLI), Jena, Germany.

Nature Communications

|July 2, 2021

Summary

The DNA damage regulator ATR protein has a novel role in non-dividing neurons. ATR deletion in neurons enhances activity, leading to increased susceptibility to ataxia and epilepsy.

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Last Updated: Oct 30, 2025

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Published on: May 25, 2011

Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

Ataxia Telangiectasia and Rad3-related (ATR) protein is a critical regulator of the DNA damage response (DDR), essential for cell viability during replication stress.
Hypomorphic mutations in ATR cause ATR-Seckel syndrome in humans, characterized by microcephaly and intellectual disability, hinting at ATR's function in non-dividing cells.

Purpose of the Study:

To investigate the role of ATR in postmitotic neurons, beyond its known function in DNA damage response.
To elucidate the mechanisms underlying ATR's influence on neuronal activity and its potential link to neurological disorders.

Main Methods:

Deletion of ATR in postmitotic neurons of mice.
Electrophysiological recordings to assess neuronal activity, action potential conformation, and synaptic vesicle dynamics.
Analysis of ATR's interaction with synaptotagmin 2 (SYT2) and its cellular localization.

Main Results:

ATR deletion in postmitotic neurons did not impair brain development but enhanced intrinsic neuronal activity, causing aberrant firing and increased epileptiform activity.
ATR-deficient neurons exhibited hyper-excitability linked to altered action potential conformation and presynaptic vesicle accumulation, independent of DDR signaling.
ATR was found to interact with SYT2; its absence led to SYT2 upregulation and aberrant translocation to excitatory hippocampal neurons, driving hyper-excitability.

Conclusions:

ATR plays a significant physiological role in regulating neuronal activity in postmitotic neurons, independent of its canonical DNA damage response functions.
Dysregulation of ATR in neurons can lead to hyperexcitability and increased susceptibility to neurological conditions like ataxia and epilepsy.
The ATR-SYT2 interaction is a key mechanism through which ATR modulates neuronal excitability.