Gonadotropin-releasing hormone regulates spine density via its regulatory role in hippocampal estrogen synthesis.
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Gonadotropin-releasing hormone regulates spine density via its regulatory role in hippocampal estrogen synthesis. / Prange-Kiel, Janine; Jarry, Hubertus; Schoen, Michael; Kohlmann, Patrick; Lohse, Christina; Zhou, Lepu; Rune, Gabriele M.
In: J CELL BIOL, Vol. 180, No. 2, 2, 2008, p. 417-426.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Gonadotropin-releasing hormone regulates spine density via its regulatory role in hippocampal estrogen synthesis.
AU - Prange-Kiel, Janine
AU - Jarry, Hubertus
AU - Schoen, Michael
AU - Kohlmann, Patrick
AU - Lohse, Christina
AU - Zhou, Lepu
AU - Rune, Gabriele M.
PY - 2008
Y1 - 2008
N2 - Spine density in the hippocampus changes during the estrus cycle and is dependent on the activity of local aromatase, the final enzyme in estrogen synthesis. In view of the abundant gonadotropin-releasing hormone receptor (GnRH-R) messenger RNA expression in the hippocampus and the direct effect of GnRH on estradiol (E2) synthesis in gonadal cells, we asked whether GnRH serves as a regulator of hippocampal E2 synthesis. In hippocampal cultures, E2 synthesis, spine synapse density, and immunoreactivity of spinophilin, a reliable spine marker, are consistently up-regulated in a dose-dependent manner at low doses of GnRH but decrease at higher doses. GnRH is ineffective in the presence of GnRH antagonists or aromatase inhibitors. Conversely, GnRH-R expression increases after inhibition of hippocampal aromatase. As we found estrus cyclicity of spine density in the hippocampus but not in the neocortex and GnRH-R expression to be fivefold higher in the hippocampus compared with the neocortex, our data strongly suggest that estrus cycle-dependent synaptogenesis in the female hippocampus results from cyclic release of GnRH.
AB - Spine density in the hippocampus changes during the estrus cycle and is dependent on the activity of local aromatase, the final enzyme in estrogen synthesis. In view of the abundant gonadotropin-releasing hormone receptor (GnRH-R) messenger RNA expression in the hippocampus and the direct effect of GnRH on estradiol (E2) synthesis in gonadal cells, we asked whether GnRH serves as a regulator of hippocampal E2 synthesis. In hippocampal cultures, E2 synthesis, spine synapse density, and immunoreactivity of spinophilin, a reliable spine marker, are consistently up-regulated in a dose-dependent manner at low doses of GnRH but decrease at higher doses. GnRH is ineffective in the presence of GnRH antagonists or aromatase inhibitors. Conversely, GnRH-R expression increases after inhibition of hippocampal aromatase. As we found estrus cyclicity of spine density in the hippocampus but not in the neocortex and GnRH-R expression to be fivefold higher in the hippocampus compared with the neocortex, our data strongly suggest that estrus cycle-dependent synaptogenesis in the female hippocampus results from cyclic release of GnRH.
M3 - SCORING: Zeitschriftenaufsatz
VL - 180
SP - 417
EP - 426
JO - J CELL BIOL
JF - J CELL BIOL
SN - 0021-9525
IS - 2
M1 - 2
ER -
