Zinc transporter 3 is involved in learned fear and extinction, but not in innate fear

Guillaume Martel, Charles Hevi, Olivia Friebely, Trevor Baybutt, Gleb P. Shumyatsky

Research output: Contribution to journalArticlepeer-review

55 Scopus citations


Synaptically released Zn2+ is a potential modulator of neurotransmission and synaptic plasticity in fear-conditioning pathways. Zinc transporter 3 (ZnT3) knock-out (KO) mice are well suited to test the role of zinc in learned fear, because ZnT3 is colocalized with synaptic zinc, responsible for its transport to synaptic vesicles, highly enriched in the amygdala-associated neural circuitry, and ZnT3 KO mice lack Zn2+ in synaptic vesicles. However, earlier work reported no deficiency in fear memory in ZnT3 KO mice, which is surprising based on the effects of Zn2+ on amygdala synaptic plasticity. We therefore reexamined ZnT3 KOmice in various tasks for learned and innate fear. The mutants were deficient in a weak fear-conditioning protocol using single tone-shock pairing but showed normal memory when a stronger, five-pairing protocol was used. ZnT3 KO mice were deficient in memory when a tone was presented as complex auditory information in a discontinuous fashion. Moreover, ZnT3 KO mice showed abnormality in trace fear conditioning and in fear extinction. By contrast, ZnT3 KO mice had normal anxiety. Thus, ZnT3 is involved in associative fear memory and extinction, but not in innate fear, consistent with the role of synaptic zinc in amygdala synaptic plasticity.

Original languageEnglish (US)
Pages (from-to)582-590
Number of pages9
JournalLearning and Memory
Issue number11
StatePublished - Nov 2010

All Science Journal Classification (ASJC) codes

  • Neuropsychology and Physiological Psychology
  • Cellular and Molecular Neuroscience
  • Cognitive Neuroscience


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