Bong‐Kiun Kaang

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 shows that protein synthesis inhibition reduces engram synapse density and spine size, impairing fear memory recall and optogenetic reactivation in mice.

This study identifies growth hormone as essential for hippocampal engram cell maturation by facilitating synaptic strengthening during memory formation.

The paper investigates brain pH and lactate levels in animal models of neuropsychiatric disorders, finding decreased pH and increased lactate levels as common features across multiple models.

This study shows that GluA1 ubiquitination at K868 is essential for LTD, spatial memory, and cognitive flexibility, but not for basal synaptic transmission or LTP.

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 provides pharmacological evidence supporting the role of CP-AMPARs in synaptic tag and capture at hippocampal CA1 synapses through experimental validation of predicted effects.

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

This study shows Shank2-/- mice have defective synapse maturation and enhanced synaptic plasticity, providing a mechanistic explanation for increased long-term potentiation.