Studies on plasticity and neurodegeneration in rat hippocampus

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.

Autorentext

Miou ZhouBachelor and Master of Science in School of Life Sciences, FudanUniversity, Shanghai, ChinaPh.D in Neuroscience at University of Southern California, USAPostdoctoral scholar in Neurobiology Program at University ofCalifornia, Los Angeles

Klappentext

Hippocampus plays an essential role in learning andmemory. Numerous studies have been directed atunderstanding the mechanisms underlying theseprocesses. In particular, the role of proteinsynthesis has been extensively debated. Hippocampusis also extremely vulnerable to numerous stressorsincluding excitotoxicity and stroke, and themechanisms underlying vulnerability of hippocampalneurons to stress are still not completelyunderstood. Studies here are concerned with bothproblems. Activity-dependent activation of excitatorysynapses results in cell membrane depolarization,calcium influx, brief activation of calcium-dependentsignaling cascades, changes in dendriticcytoskeleton and protein synthesis; on the otherhand, excessive activation of excitatory synapseselicits excessive calcium influx, prolongedactivation of calcium-dependent proteases such ascalpain, breakdown of calcium homeostasis andneuronal damage. While my studies cover bothneurodegeneration and synaptic plasticity, the commonpathways they share suggest that depending onactivation conditions, the same pathway might act ondistinct substrates and produce quite different results.