Ji‐il Kim

The paper shows that synaptic depression between memory-encoding engram cells impairs memory, demonstrating that synaptic plasticity between these cells causally supports memory.

This study creates human neuromodulatory assembloids to investigate serotonin signaling and disease mechanisms, showing altered 5-HT dynamics in 22q11.2DS and rescue with SSRIs.

The paper develops a human midline assembloid model to study axon guidance and identifies GALNT2 as a human-specific regulator of commissural axon guidance.

This study creates a human assembloid model of the ascending somatosensory pathway using pluripotent stem cells and demonstrates its functional connectivity and response to pain-related stimuli.

The paper develops an assembloid model of the human cortico-striatal-thalamic-cortical circuit to study its function and disease-related disruptions.

This study uses human assembloids to investigate how CACNA1G gene variants affect thalamocortical pathway function in neuropsychiatric disorders.

The paper shows that astrocytes form more connections with engram neurons after learning, and these connections are stabilized by neuronal activity.

This study tracks synaptic changes in the hippocampus during fear memory formation and extinction, showing synaptogenesis and synapse modification between CA3 and CA1 engram cells.

This study functionally characterizes a neuropeptide receptor in Aplysia neurons by expressing it exogenously and demonstrating its role in modulating neuronal excitability.

The paper shows that associative fear memory increases spine size at synapses between engram cells in the amygdala, which decreases with extinction and recovers with re-conditioning.

The paper shows that LTP in hippocampal synapses can increase AMPA receptor number or conductance, with distinct mechanisms involving CaMKII and PKA.