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CTRP4 ablation impairs associative learning and memory.

Dylan C Sarver¹, Cheng Xu¹, Yi Cheng¹

¹Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology

|October 5, 2021

Summary

This summary is machine-generated.

C1q/TNF-related protein 4 (CTRP4) deficiency in mice alters pain sensitivity and impairs hippocampal-dependent learning and memory, particularly in females. These findings reveal new central nervous system roles for CTRP4.

Keywords:

C1QTNF4 cortex hippocampus learning and memory mouse behavior secreted hormone

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Area of Science:

Neuroscience
Metabolic regulation
Genetics

Background:

The C1q/TNF-related protein (CTRP) family has diverse functions, with CTRP4 highly expressed in the brain.
Previous studies identified CTRP4 as a regulator of food intake and energy balance, with sexually dimorphic effects in mice.
Single-cell RNA sequencing indicated Ctrp4 expression in various brain cell types, suggesting uncharacterized central nervous system roles.

Purpose of the Study:

To investigate the novel central nervous system functions of CTRP4.
To characterize the behavioral and physiological consequences of CTRP4 deficiency in mice.

Main Methods:

Utilized Ctrp4 knockout (KO) mice and wild-type (WT) littermates.
Conducted a comprehensive battery of behavioral tests assessing exploratory, anxiety-, depressive-like behaviors, motor function, sensorimotor gating, recognition, and spatial memory.
Evaluated nociceptive function using thermal and shock-induced pain paradigms.
Assessed hippocampal-dependent associative learning and memory via trace fear conditioning.
Analyzed gene expression of learning and memory markers in the hippocampus and cortex.

Main Results:

CTRP4 deficiency did not affect general behaviors like exploration, anxiety, depression, motor control, or basic memory functions.
Ctrp4 KO mice exhibited increased sensitivity to higher-level shock-induced pain in both sexes.
CTRP4 deficiency specifically impaired hippocampal-dependent associative learning and memory in female mice.
This learning deficit in females was linked to altered expression of learning and memory genes (Arc, c-fos, Pde4d) in the brain.

Conclusions:

CTRP4 plays a significant role in central nervous system functions beyond metabolic regulation.
CTRP4 influences nociception and is critical for hippocampal-dependent associative learning, with a sex-specific effect in females.
These findings provide a foundation for further research into CTRP4's mechanisms in the central and peripheral nervous systems.