Physiology studies demonstrate that CaMKII is a molecular storage device.

Electrophysiological and optical analysis of neurotransmitter release at central synapses reveals that glutamate signalling is not required for the long-term potentiation (LTP) of presynaptic function, and instead only promotes presynaptic long-term depression (LTD).

Vulnerability to cocaine addiction during adolescence depends on translational control.

Non-invasive optogenetic induction of synaptic plasticity revealed that long-term potentiation and long-term depression alter the chances of a synapse to survive the next seven days.

There are at least two separate pathways for AMPA receptor recycling, which are regulated by synaptic activity.

Group III metabotropic glutamate receptor inhibition facilitates synaptic plasticity in the plasticity-resistant synapses of hippocampal area CA2, a brain region critical for social memory.

The secretory and recycling components of neuronal dendrites, smooth endoplasmic reticulum and endosomes, were discovered to support synaptogenesis underlying a cellular mechanism of learning and memory in the developing brain.

The molecular mechanisms beyond the bidirectionality (tTLP and tLTD) of endocanabinoid spike-timing dependent synaptic plasticity have been identified.

Behavioral analyses and an optogenetic approach reveal an existence of GR-mediated metaplasticity in the LA and its link with adaptive fear response to auditory cues in a stressful condition.

Mouse models with specific presynaptic knockout demonstrate that Rim1α is subjected to threonine phosphorylation by a novel EPAC-PKCε module, which is essential to presynaptic transmitter release, required for the induction of presynaptic LTP, and critical for motor learning.