Hippocampus plays an essential role in learning and
memory. Numerous studies have been directed at
understanding the mechanisms underlying these
processes. In particular, the role of protein
synthesis has been extensively debated. Hippocampus
is also extremely vulnerable to numerous stressors
including excitotoxicity and stroke, and the
mechanisms underlying vulnerability of hippocampal
neurons to stress are still not completely
understood. Studies here are concerned with both
problems. Activity-dependent activation of excitatory
synapses results in cell membrane depolarization,
calcium influx, brief activation of calcium-dependent
signaling cascades, changes in dendritic
cytoskeleton and protein synthesis; on the other
hand, excessive activation of excitatory synapses
elicits excessive calcium influx, prolonged
activation of calcium-dependent proteases such as
calpain, breakdown of calcium homeostasis and
neuronal damage. While my studies cover both
neurodegeneration and synaptic plasticity, the common
pathways they share suggest that depending on
activation conditions, the same pathway might act on
distinct substrates and produce quite different results.
memory. Numerous studies have been directed at
understanding the mechanisms underlying these
processes. In particular, the role of protein
synthesis has been extensively debated. Hippocampus
is also extremely vulnerable to numerous stressors
including excitotoxicity and stroke, and the
mechanisms underlying vulnerability of hippocampal
neurons to stress are still not completely
understood. Studies here are concerned with both
problems. Activity-dependent activation of excitatory
synapses results in cell membrane depolarization,
calcium influx, brief activation of calcium-dependent
signaling cascades, changes in dendritic
cytoskeleton and protein synthesis; on the other
hand, excessive activation of excitatory synapses
elicits excessive calcium influx, prolonged
activation of calcium-dependent proteases such as
calpain, breakdown of calcium homeostasis and
neuronal damage. While my studies cover both
neurodegeneration and synaptic plasticity, the common
pathways they share suggest that depending on
activation conditions, the same pathway might act on
distinct substrates and produce quite different results.