The unique expression profile of FAM19A1 in the mouse brain and its association with hyperactivity, long-term memory and fear acquisition

• Published in: Scientific reports 2020-03, Vol.10 (1), p.3969, Article 3969
• Main Authors: Yong, Hyo Jeong, Ha, Nui, Cho, Eun Bee, Yun, Seongsik, Kim, Hyun, Hwang, Jong-Ik, Seong, Jae Young
• Format: Article
• Language: English
• Subjects: 14/19; 631/378/1689/2608; 631/378/2571/1696; 64/110; Amino acid sequence; Amino acids; Amygdala; Amygdala - metabolism; Animals; Behavior, Animal; Brain; Brain - metabolism; Cerebral cortex; Chemokines; Chemokines - physiology; Conditioning, Psychological; Conserved sequence; Cytokines; Embryogenesis; Fear; Fear - physiology; Female; Hippocampus - metabolism; Humanities and Social Sciences; Hyperactivity; Hyperkinesis - physiopathology; Long term memory; Male; Memory, Long-Term - physiology; Mice; Mice, Knockout; multidisciplinary; Neurodevelopment; Physiology; Pyramidal cells; Reporter gene; Rodents; Science; Science (multidisciplinary)
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-020-60266-1

Neurodevelopment and mature brain function are spatiotemporally regulated by various cytokines and chemokines. The chemokine-like neuropeptide FAM19A1 is a member of family with sequence similarity 19 (FAM19), which is predominantly expressed in the brain. Its highly conserved amino acid sequence among vertebrates suggests that FAM19A1 may play important physiological roles in neurodevelopment and brain function. Here we used a LacZ reporter gene system to map the expression pattern of the FAM19A1 gene in the mouse brain. The FAM19A1 expression was observed in several brain regions starting during embryonic brain development. As the brain matured, the FAM19A1 expression was detected in the pyramidal cells of cortical layers 2/3 and 5 and in several limbic areas, including the hippocampus and the amygdala. FAM19A1-deficient mice were used to evaluate the physiological contribution of FAM19A1 to various brain functions. In behavior analysis, FAM19A1-deficient mice exhibited several abnormal behaviors, including hyperactive locomotor behavior, long-term memory deficits and fear acquisition failure. These findings provide insight into the potential contributions of FAM19A1 to neurodevelopment and mature brain function.