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Estrus cyclicity of spinogenesis: underlying mechanisms

Hippocampal spine density varies with the estrus cycle. The cyclic change in estradiol levels in serum was hypothesized to underlie this phenomenon, since treatment of ovariectomized animals with estradiol induced an increase in spine density in hippocampal dendrites of rats, as compared to ovariect...

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Autores principales: Prange-Kiel, Janine, Fester, Lars, Zhou, Lepu, Jarry, Hubertus, Rune, Gabriele M.
Formato: Texto
Lenguaje:English
Publicado: Springer Vienna 2009
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085745/
https://www.ncbi.nlm.nih.gov/pubmed/19730783
http://dx.doi.org/10.1007/s00702-009-0294-x
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author Prange-Kiel, Janine
Fester, Lars
Zhou, Lepu
Jarry, Hubertus
Rune, Gabriele M.
author_facet Prange-Kiel, Janine
Fester, Lars
Zhou, Lepu
Jarry, Hubertus
Rune, Gabriele M.
author_sort Prange-Kiel, Janine
collection PubMed
description Hippocampal spine density varies with the estrus cycle. The cyclic change in estradiol levels in serum was hypothesized to underlie this phenomenon, since treatment of ovariectomized animals with estradiol induced an increase in spine density in hippocampal dendrites of rats, as compared to ovariectomized controls. In contrast, application of estradiol to hippocampal slice cultures did not promote spinogenesis. In addressing this discrepancy, we found that hippocampal neurons themselves are capable of synthesizing estradiol de novo. Estradiol synthesis can be suppressed by aromatase inhibitors and by knock-down of Steroid Acute Regulatory Protein (StAR) and enhanced by substrates of steroidogenesis. Expression of estrogen receptors (ERs) and synaptic proteins, synaptogenesis, and long-term potentiation (LTP) correlated positively with aromatase activity in hippocampal cultures without any difference between genders. All effects due to inhibition of aromatase activity were rescued by application of estradiol to the cultures. Most importantly, gonadotropin-releasing hormone (GnRH) increased estradiol synthesis dose-dependently via an aromatase-mediated mechanism and consistently increased spine synapse density and spinophilin expression. As a consequence, our data suggest that cyclic fluctuations in spine synapse density result from pulsative release of GnRH from the hypothalamus and its effect on hippocampal estradiol synthesis, rather than from varying levels of serum estradiol. This hypothesis is further supported by higher GnRH receptor (GnRH-R) density in the hippocampus than in the cortex and hypothalamus and the specificity of estrus cyclicity of spinogenesis in the hippocampus, as compared to the cortex.
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spelling pubmed-30857452011-06-06 Estrus cyclicity of spinogenesis: underlying mechanisms Prange-Kiel, Janine Fester, Lars Zhou, Lepu Jarry, Hubertus Rune, Gabriele M. J Neural Transm Basic Neurosciences, Genetics and Immunology - Original Article Hippocampal spine density varies with the estrus cycle. The cyclic change in estradiol levels in serum was hypothesized to underlie this phenomenon, since treatment of ovariectomized animals with estradiol induced an increase in spine density in hippocampal dendrites of rats, as compared to ovariectomized controls. In contrast, application of estradiol to hippocampal slice cultures did not promote spinogenesis. In addressing this discrepancy, we found that hippocampal neurons themselves are capable of synthesizing estradiol de novo. Estradiol synthesis can be suppressed by aromatase inhibitors and by knock-down of Steroid Acute Regulatory Protein (StAR) and enhanced by substrates of steroidogenesis. Expression of estrogen receptors (ERs) and synaptic proteins, synaptogenesis, and long-term potentiation (LTP) correlated positively with aromatase activity in hippocampal cultures without any difference between genders. All effects due to inhibition of aromatase activity were rescued by application of estradiol to the cultures. Most importantly, gonadotropin-releasing hormone (GnRH) increased estradiol synthesis dose-dependently via an aromatase-mediated mechanism and consistently increased spine synapse density and spinophilin expression. As a consequence, our data suggest that cyclic fluctuations in spine synapse density result from pulsative release of GnRH from the hypothalamus and its effect on hippocampal estradiol synthesis, rather than from varying levels of serum estradiol. This hypothesis is further supported by higher GnRH receptor (GnRH-R) density in the hippocampus than in the cortex and hypothalamus and the specificity of estrus cyclicity of spinogenesis in the hippocampus, as compared to the cortex. Springer Vienna 2009-09-04 2009-11 /pmc/articles/PMC3085745/ /pubmed/19730783 http://dx.doi.org/10.1007/s00702-009-0294-x Text en © Springer-Verlag 2009
spellingShingle Basic Neurosciences, Genetics and Immunology - Original Article
Prange-Kiel, Janine
Fester, Lars
Zhou, Lepu
Jarry, Hubertus
Rune, Gabriele M.
Estrus cyclicity of spinogenesis: underlying mechanisms
title Estrus cyclicity of spinogenesis: underlying mechanisms
title_full Estrus cyclicity of spinogenesis: underlying mechanisms
title_fullStr Estrus cyclicity of spinogenesis: underlying mechanisms
title_full_unstemmed Estrus cyclicity of spinogenesis: underlying mechanisms
title_short Estrus cyclicity of spinogenesis: underlying mechanisms
title_sort estrus cyclicity of spinogenesis: underlying mechanisms
topic Basic Neurosciences, Genetics and Immunology - Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3085745/
https://www.ncbi.nlm.nih.gov/pubmed/19730783
http://dx.doi.org/10.1007/s00702-009-0294-x
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