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Real-Time Fluorescent Measurement of Synaptic Functions in Models of Amyotrophic Lateral Sclerosis
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Motoneurons Inhibitory Synapses Homeostatically Respond to Neuronal Activity and Modulate Amyotrophic Lateral

Kareen Halablab1,2, Gizem Yartas1, Natalie Dikwella2

  • 1German Center for Neurodegenerative Diseases (DZNE), Ulm 89081, Germany.

The Journal of Neuroscience : the Official Journal of the Society for Neuroscience
|March 12, 2026
PubMed
Summary
This summary is machine-generated.

Inhibitory synapses in motor neurons (MN) adapt to changes in MN activity during early ALS. Suppressing these inhibitory connections increases MN excitability and reduces disease markers, suggesting therapeutic potential.

Keywords:
amyotrophic lateral sclerosischemogeneticsexcitationinhibitory synapsesintrabodiesmotoneurons

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Area of Science:

  • Neuroscience
  • Neurodegenerative Diseases
  • Synaptic Plasticity

Background:

  • Motor neuron (MN) vulnerability in Amyotrophic Lateral Sclerosis (ALS) may involve altered excitation/inhibition (E/I) balance.
  • The role of adaptive changes in inhibitory synapses during early ALS pathogenesis remains unclear.

Purpose of the Study:

  • To investigate the dynamic changes in inhibitory synapses onto MN in early ALS.
  • To explore the homeostatic responses of inhibitory synapses to MN activity modulation.
  • To assess the impact of modulating inhibitory synaptic components on ALS disease markers.

Main Methods:

  • Confocal microscopy of MN from SOD1G93A mice.
  • Chemogenetic tools (PSAM, DREADD) to alter MN excitability.
  • An E3 ligase-conjugated intrabody (GFE3) to degrade Gephyrin and reduce inhibitory receptor clusters.

Main Results:

  • Downregulation of GlyR and upregulation of GABAR clusters observed at inhibitory synapses in MN.
  • Inhibitory synapses showed homeostatic responses, increasing clusters with heightened MN activity.
  • GFE3 treatment decreased inhibitory clusters, increased net MN activity, and reduced disease markers.
  • Combined activity increase and inhibition decrease did not yield net beneficial effects on disease markers.

Conclusions:

  • Inhibitory synapses are dynamically involved in early ALS pathogenesis and exhibit homeostatic regulation.
  • Suppression of inhibitory synapses increases net MN activity, potentially impacting disease pathways.
  • Modulating inhibitory synaptic components offers a potential therapeutic avenue for ALS.