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Estrogen induces rapid decrease in dendritic thorns of CA3 pyramidal neurons in adult male rat hippocampus
Tomokazu Tsurugizawa1, Hideo Mukai, Nobuaki Tanabe
1Department of Biophysics and Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo at Komaba, 3-8-1 Meguro, Tokyo 153, Japan.
Biochemical and Biophysical Research Communications
|October 26, 2005
Summary
Estradiol rapidly reduces the density of CA3 hippocampal neuron thorns, a key synaptic plasticity site. This effect involves estrogen receptor alpha (ERalpha) and the MAP kinase pathway, not NMDA receptors.
Area of Science:
- Neuroscience
- Cell Biology
- Endocrinology
Background:
- Estrogen's role in modulating hippocampal synaptic plasticity is a significant area of research.
- Thorny excrescences on CA3 hippocampal neurons are postsynaptic sites receiving input from mossy fiber terminals.
Purpose of the Study:
- To investigate the rapid effects of estradiol on the density of thorns in CA3 hippocampal neurons.
- To elucidate the signaling pathways involved in estradiol-mediated modulation of synaptic structures.
Main Methods:
- Imaging of Lucifer Yellow-injected CA3 neurons in adult male rat hippocampal slices.
- Application of estradiol and specific receptor antagonists (CNQX, PD98059, MK-801) and agonists (PPT, DPN).
- Immunogold electron microscopy to determine the localization of estrogen receptor alpha (ERalpha).
Main Results:
- A rapid decrease in thorn density on CA3 pyramidal neurons was observed within 2 hours of 1nM estradiol application.
- The estradiol effect was blocked by AMPA receptor antagonist CNQX and MAP kinase inhibitor PD98059, but not NMDA receptor antagonist MK-801.
- ERalpha agonist PPT mimicked estradiol's effect, while ERbeta agonist DPN did not; ERalpha was localized in CA3 mossy fiber terminals and thorns.
Conclusions:
- Estradiol rapidly decreases the density of CA3 hippocampal thorns, suggesting a role in synaptic plasticity modulation.
- The signaling pathway involves ERalpha and MAP kinase, with AMPA receptors playing a role, but not NMDA receptors.
- These findings highlight a specific mechanism for estrogen's rapid action on neuronal structure and function.