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ABLATION OF COPPER TRANSPORTER 1 INDUCES COGNITIVE AND EMOTIONAL ALTERATIONS THROUGH MITOCHONDRIAL DYSFUNCTION IN MICE
Jeongmin Leeand 5 co-authors
College of Veterinary Medicine and BK21 FOUR Program, Chonnam National University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS06-09PM-173
Presentation
Date TBA
Board: PS06-09PM-173
Event Information
Poster Board
PS06-09PM-173
Poster
View posterAbstract
Copper serves as an essential trace element in the brain, playing significant roles in neurotransmitter synthesis, connective tissue synthesis, neuropeptide activation, and energy production. Although extensive research has been conducted on copper metabolism, the potential involvement of copper transporters in brain function is still inadequately understood. Here, we investigated behavioral and molecular alterations in nestin-specific copper transporter 1 (Ctr1) conditional knockout (cKO) mice. Ctr1-cKO mice exhibited cognitive impairment (memory deficits in the passive avoidance test) and affective dysregulation (increased anxiety-like behavior in the open field test and enhanced depression-like behavior in the tail suspension test). Consistently, levels of neuroplasticity-associated proteins, including phosphorylated ERK (pERK) and c-Fos, as well as mitochondrial complex IV activity, were reduced in the hippocampus of Ctr1-cKO mice. In primary hippocampal neuronal cultures derived from Ctr1-floxed mice, Adv-GFP/Cre infection markedly altered the oxygen consumption rate. Collectively, these findings suggest that Ctr1 deletion compromises neuroplasticity and mitochondrial function, thereby contributing to cognitive deficits and emotional dysregulation in mice.
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