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Zinc (Zn 2+ ) is a pleiotropic modulator of the neuronal and brain activity. The disruption of intraneuronal Zn 2+  levels triggers neurotoxic processes and affects neuronal functioning. In this study, we investigated how the pharmacological modulation of brain Zn 2+  affects synaptic plasticity and cognition in wild-type mice. To manipulate brain Zn 2+  levels, we employed the Zn 2+  (and copper) chelator 5-chloro-7-iodo-8-hydroxyquinoline (clioquinol, CQ). CQ was administered for two weeks to 2.5-month-old (m.o.) mice, and effects studied on BDNF-related signaling, metalloproteinase activity as well as learning and memory performances. CQ treatment was found to negatively affect short- and long-term memory performances. The CQ-driven perturbation of brain Zn 2+  was found to reduce levels of BDNF, synaptic plasticity-related proteins and dendritic spine density  in vivo . Our study highlights the importance of choosing “when”, “where”, and “how much” in the modulation of brain Zn 2+  levels. Our findings confirm the importance of targeting Zn 2+  as a therapeutic approach against neurodegenerative conditions but, at the same time, underscore the potential drawbacks of reducing brain Zn 2+  availability upon the early stages of development.

The pharmacological perturbation of brain zinc impairs BDNF-related signaling and the cognitive performances of young mice