A specific role for hippocampal mossy fiber's zinc in rapid storage of emotional memories

Abstract

We investigated the specific role of zinc present in large amounts in the synaptic vesicles of mossy fibers and coreleased with glutamate in the CA3 region. In previous studies, we have shown that blockade of zinc after release has no effect on the consolidation of spatial learning, while zinc is required for the consolidation of contextual fear conditioning. Although both are hippocampo-dependent processes, fear conditioning to the context implies a strong emotional burden. To verify the hypothesis that zinc could play a specific role in enabling sustainable memorization of a single event with a strong emotional component, we used a neuropharmacological approach combining a glutamate receptor antagonist with different zinc chelators. Results show that zinc is mandatory to allow the consolidation of one-shot memory, thus being the key element allowing the hippocampus submitted to a strong emotional charge to switch from the cognitive mode to a flashbulb memory mode. Individual differences in learning abilities have been known for a long time to be totally or partially compensated by distributed learning practice. Here we show that contextual fear conditioning impairments due to zinc blockade can be efficiently reduced by distributed learning practice.

The Rapid Exchange of Zinc2+ Enables Trace Levels to Profoundly Influence Amyloid-β Misfolding and Dominates Assembly Outcomes in Cu2+/Zn2+ Mixtures

“…Zn 2+ is an important intracellular signalling molecule that is thought to be crucial for synaptic plasticity, learning, and memory [9][10][11]. In the brain, large reserves of free Zn 2+ are found to be stored in the presynaptic vesicles of glutamatergic neurons, transported there by Zinc transporter-3 (ZnT3) [12][13][14][15].…”

CAPS1 is involved in hippocampal synaptic plasticity and hippocampus-associated learning

“…In CA1, not only the abnormal LTP magnitude, but also the low level of basal synaptic transmission is involved in the behavioral results. Conversely, the severe impairment of CA3 LTP induction should affect the learning performance, because dentate gyrus and CA3 neurons are required for CFC learning and memory [38][39][40][41] . In addition, CAPS1 deficits in axonal terminals may reduce synaptic input from the hippocampus to other brain areas such as the entorhinal cortex, which may also contribute to learning impairments.…”

Resolving the Ultrastructural Organization of Synaptic Vesicle Pools at Hippocampal Mossy Fiber and Schaffer Collateral Synapses

“…where they form synaptic connections with pyramidal neurons (Figure 3 A) (Blackstad and Kjaerheim, 1961). Outgoing axonal projections run from the CA1 to layer V neurons in the EC via subiculum (Ceccom et al, 2014).…”