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Complement Component C3 Loss leads to Locomotor Deficits and Altered Cerebellar Internal Granule Cell In Vitro
Nicholas W DeKorver1, Tammy R Chaudoin1, Gang Zhao2
1Department of Internal Medicine, Division of Geriatrics, University of Nebraska Medical Center, 3028 Durham Research Center II, Omaha, NE, 68198-5039, USA.
Molecular Neurobiology
|August 20, 2021
Summary
Complement component 3 (C3) loss in mice impairs locomotion, causing gait ataxia. This suggests C3 is crucial for cerebellar control of movement and excitatory synapse function.
Area of Science:
- Neuroscience
- Immunology
Background:
- Complement component 3 (C3) expression elevates in aging mouse cerebellums with locomotor deficits.
- C3's precise roles in locomotion and excitatory synapse regulation are unclear.
Purpose of the Study:
- Investigate C3's function in cerebellar-mediated locomotion.
- Determine C3's impact on excitatory synapse density and function.
Main Methods:
- Generated constitutive C3 knockout mice.
- Assessed locomotor behavior and gait.
- Analyzed cerebellar excitatory synaptic density in vivo and in vitro.
- Examined muscle and joint health.
Main Results:
- C3 knockout mice exhibited decreased speed, increased active locomotor probability, and ataxia.
- C3 loss did not affect metabolism, body composition, muscle strength, or arthritis.
- In vitro, C3 deficiency increased cerebellar granule cell excitatory synaptic density and excitability.
- In vivo, cerebellar synaptic density remained unchanged, suggesting compensatory mechanisms.
Conclusions:
- C3 plays a novel role in the cerebellum's regulation of locomotor output.
- Locomotor deficits in C3 knockout mice likely stem from altered synaptic function/connectivity, not gross deficits.
