Synaptic plasticity in the hippocampus: effects of estrogen from the gonads or hippocampus?
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Synaptic plasticity in the hippocampus: effects of estrogen from the gonads or hippocampus? / Rune, G M; Lohse, C; Prange-Kiel, Janine; Fester, Lars; Frotscher, M.
In: NEUROCHEM RES, Vol. 31, No. 2, 2, 2006, p. 145-155.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Synaptic plasticity in the hippocampus: effects of estrogen from the gonads or hippocampus?
AU - Rune, G M
AU - Lohse, C
AU - Prange-Kiel, Janine
AU - Fester, Lars
AU - Frotscher, M
PY - 2006
Y1 - 2006
N2 - Different effects of estrogen on synaptic plasticity have [corrected] been reported. Here, we summarise effects of low, gonad-derived serum estrogen concentrations, of intermediate concentrations, provided by hippocampal cells, and of pharmacological doses of estrogen on synapses and spines and on the expression of synaptic proteins. No effects of low concentrations were found. To study the effects of hippocampus-derived estradiol, we inhibited hippocampal estrogen synthesis by treatment of hippocampal cell cultures with letrozole, an aromatase inhibitor. Alternatively, we used siRNA against Steroidogenic acute regulatory protein (StAR). Spines, synapses, and synaptic proteins were significantly down regulated in response to letrozole and in siRNA-StAR transfected cells. Application of high pharmacological doses of estradiol promoted only synaptophysin expression, a presynaptic protein, but did not increase the number of boutons. Our results point to an essential role of endogenous hippocampal estrogen in hippocampal synaptic plasticity rather than to a direct influence of estrogens derived from peripheral sources, such as the gonads.
AB - Different effects of estrogen on synaptic plasticity have [corrected] been reported. Here, we summarise effects of low, gonad-derived serum estrogen concentrations, of intermediate concentrations, provided by hippocampal cells, and of pharmacological doses of estrogen on synapses and spines and on the expression of synaptic proteins. No effects of low concentrations were found. To study the effects of hippocampus-derived estradiol, we inhibited hippocampal estrogen synthesis by treatment of hippocampal cell cultures with letrozole, an aromatase inhibitor. Alternatively, we used siRNA against Steroidogenic acute regulatory protein (StAR). Spines, synapses, and synaptic proteins were significantly down regulated in response to letrozole and in siRNA-StAR transfected cells. Application of high pharmacological doses of estradiol promoted only synaptophysin expression, a presynaptic protein, but did not increase the number of boutons. Our results point to an essential role of endogenous hippocampal estrogen in hippocampal synaptic plasticity rather than to a direct influence of estrogens derived from peripheral sources, such as the gonads.
M3 - SCORING: Zeitschriftenaufsatz
VL - 31
SP - 145
EP - 155
JO - NEUROCHEM RES
JF - NEUROCHEM RES
SN - 0364-3190
IS - 2
M1 - 2
ER -