Sex Steroids and Synaptic
Plasticity in Aging
Caleb E.
Finch, Ph.D. Director
Irina Rozovsky, Ph.D. Co-director
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Rozovsky I., Wei M., Stone D.J., Zanjani H., Anderson C.P., Morgan T.E., and Finch C.E., Estradiol (E2) Enhances Neurite Outgrowth by Repressing Glial Fibrilary Acidic Protein Expression and Reorganizing Laminin. Endocrinology 143(2):636-646
This project addresses steroidal
influences on synaptic remodeling in the rodent brain in vivo and in vitro with
cell culture models, with a focus on astrocyte genes that are regulated by
estradiol and corticosterone.
Specific Studies
1. Transcriptional
regulation of GFAP in astrocytes and of genes expressed in neurons that show
modulation by estradiol using in vitro cell models for response to estradiol,
corticosterone and injury.
2. Effects
of estradiol on synaptic plasticity in hippocampus with markers for synaptic
remodeling in astrocytes and neurons using in vivo gene expression.
3. Effects
of aging on interactions of estradiol and synaptic plasticity in vivo.
Main findings:
1. In the entorhinal cortex
lesion (ECL) model of hippocampal deafferentation during
Alzheimer, we showed in female mice that
estradiol (E2) enhanced synaptophysin as
a marker for neuron sprouting (Stone et
al Endocrinology 1998). Moreover, this effect of E2 was attenuated
in apoE-deficient mice (Stone et al J Neurosci 1998), consistent with
prior studies showing that E2 induced apoE mRNA and secretions by astrocytes
(Stone et al. Exp Neurol 1997). These results directly
show the importance of apoE in E2-sensitive sprouting and are consistent with
the impairments of synaptic plasticity in apoE deficient mice, more generally.
2. E2 and apoE: Bioactivities of
Premarin components Equilin induces apoE mRNA and secretion in cultured
glia at the same sensitivity as E2 (Rozovsky et al, in prep). This
finding is consistent with positive effects of equilin on neuron outgrowth in
culture by Brinton et al. Exp Neurol 1997].
3. Two new responses to E2:
mRNAs for the presynaptic proteins synaptotagmin I and synaptophysin, which
also vary during the estrous cycle (Crispino et al., Exp Neurol
1999); collaboration with Project 4.
4. Effects of estrogens on the
GFAP gene which influences the environment of neurons by changing the shape
of astrocytes that surround the synapses of neurons.
a. The regulation of GFAP by
estradiol depends on an estrogen response element (ERE) in the near upstream
promoter, as shown by site directed mutagenesis and by the binding of
estrogen receptor alpha to this ERE (Stone et al., Endocrinology 1998).
b. As a model for complex cell
interactions of E2 in vivo, we developed the wounding in a dish model in which
neurons are grown over a layer of astrocytes. Astrocytes showed robust
induction of GFAP transcription by wounding that was blocked by E2. GFAP
promoter regions were identified that mediate responses to wounding and
interactions with E2 (Rozovsky et al., submitted). E2 also enhanced neuronal
sprouting and extracellular laminin reorganization. Previously,
Lefrancoise et al (J Neuroscience 1997) shown in this same model that
down regulation of GFAP mRNA and protein by antisense GFAP had exactly the same
effect as E2 on sprouting and laminin. Thus, in two examples,
inhibition of GFAP is sufficient for enhancing sprouting by reorganization of
laminin. This is the first indication that brain laminin is controlled by sex
steroids. We hypothesize that E2
regulates a cascade of astrocyte cytoskeletal proteins through GFAP
transcription, with downstream effects on laminin and, in turn, on neurite
outgrowth.
__________________________________________________
Caleb E. Finch, Ph.D. (PI)
cfinch@molbio.usc.edu
Irina Rozovsky, Ph.D.
rozovsky@molbio.usc.edu
Christopher P. Anderson, Ph.D.
cpanders@molbio.usc.edu
Todd Morgan
temorgan@usc.edu
Estrogen
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