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C1ql3 knockout affects microglia activation, neuronal integrity, and spontaneous behavior in Wistar rats
Li Zhang1, Wei Dong2, Jingwen Li2
1Beijing Engineering Research Center for Experimental Animal Models of Human Diseases, Institute of Laboratory Animal Science, Peking Union Medicine College, Chinese Academy of Medical Sciences, Beijing, China.
Animal Models and Experimental Medicine
|February 21, 2024
Summary
Complement component 1 Q like 3 (C1QL3) deficiency in rats impairs neuronal integrity and alters microglial activation. This leads to hyperactivity and deficits in short-term memory, highlighting C1QL3's role in brain cell regulation.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- C1QL3 is expressed in excitatory neurons but its function remains unclear.
- C1QL3-deficient rats were created to investigate its role in the brain.
- Understanding C1QL3's function is crucial for brain health.
Purpose of the Study:
- To investigate the function of C1QL3 in the brain.
- To analyze the effects of C1QL3 deficiency on neuronal and microglial cells.
- To evaluate behavioral changes in C1QL3 knockout rats.
Main Methods:
- C1QL3 knockout rats were generated using CRISPR/Cas9.
- Microglia morphology, cytokine expression, brain structure, and neuronal architecture were analyzed.
- Behavioral tests including open field, Morris water maze, and Y maze were performed.
Main Results:
- C1QL3 knockout altered microglia morphology and increased Arg-1 expression post-LPS stimulation.
- Neuronal integrity was compromised, affecting dendritic arbors and spine density.
- C1QL3 knockout rats exhibited increased spontaneous activity and impaired short-term memory.
Conclusions:
- C1QL3 deficiency disrupts neuronal integrity and affects microglial activation.
- These disruptions result in hyperactive behavior and impaired short-term memory in rats.
- C1QL3 plays a significant role in regulating the structure and function of neuronal and microglial cells.
