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The neuroprotective effects of 17β-estradiol pretreatment in a model of neonatal hippocampal injury induced by trimethyltin

Marchese, Elisa; Corvino, Valentina; Di Maria, Valentina LU ; Furno, Alfredo; Giannetti, Stefano; Cesari, Eleonora; Lulli, Paola; Michetti, Fabrizio and Geloso, Maria Concetta (2018) In Frontiers in Cellular Neuroscience 12.
Abstract

Hippocampal dysfunction plays a central role in neurodevelopmental disorders, resulting in severe impairment of cognitive abilities, including memory and learning. On this basis, developmental studies represent an important tool both to understanding the cellular and molecular phenomena underlying early hippocampal damage and to study possible therapeutic interventions, that may modify the progression of neuronal death. Given the modulatory role played by 17β-estradiol (E2) on hippocampal functions and its neuroprotective properties, the present study investigates the effects of pretreatment with E2 in a model of neonatal hippocampal injury obtained by trimethyltin (TMT) administration, characterized by neuronal loss in CA1 and CA3... (More)

Hippocampal dysfunction plays a central role in neurodevelopmental disorders, resulting in severe impairment of cognitive abilities, including memory and learning. On this basis, developmental studies represent an important tool both to understanding the cellular and molecular phenomena underlying early hippocampal damage and to study possible therapeutic interventions, that may modify the progression of neuronal death. Given the modulatory role played by 17β-estradiol (E2) on hippocampal functions and its neuroprotective properties, the present study investigates the effects of pretreatment with E2 in a model of neonatal hippocampal injury obtained by trimethyltin (TMT) administration, characterized by neuronal loss in CA1 and CA3 subfields and astroglial and microglial activation. At post-natal days (P)5 and P6 animals received E2 administration (0.2 mg/kg/die i.p.) or vehicle. At P7 they received a single dose of TMT (6.5 mg/kg i.p.) and were sacrificed 72 h (P10) or 7 days after TMT treatment (P14). Our findings indicate that pretreatment with E2 exerts a protective effect against hippocampal damage induced by TMT administration early in development, reducing the extent of neuronal death in the CA1 subfield, inducing the activation of genes involved in neuroprotection, lowering the neuroinflammatory response and restoring neuropeptide Y- and parvalbumin- expression, which is impaired in the early phases of TMT-induced damage. Our data support the efficacy of estrogen-based neuroprotective approaches to counteract early occurring hippocampal damage in the developing hippocampus.

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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Estrogen, Hippocampus, Neuroinflammation, Neuroprotection, Post-natal development, Trimethyltin
in
Frontiers in Cellular Neuroscience
volume
12
publisher
Frontiers
external identifiers
  • scopus:85056825623
ISSN
1662-5102
DOI
10.3389/fncel.2018.00385
language
English
LU publication?
yes
id
1eac1d81-2ea8-4a8b-9b02-f5d40bab92fb
date added to LUP
2018-11-29 14:05:42
date last changed
2019-02-20 11:38:24
@article{1eac1d81-2ea8-4a8b-9b02-f5d40bab92fb,
  abstract     = {<p>Hippocampal dysfunction plays a central role in neurodevelopmental disorders, resulting in severe impairment of cognitive abilities, including memory and learning. On this basis, developmental studies represent an important tool both to understanding the cellular and molecular phenomena underlying early hippocampal damage and to study possible therapeutic interventions, that may modify the progression of neuronal death. Given the modulatory role played by 17β-estradiol (E2) on hippocampal functions and its neuroprotective properties, the present study investigates the effects of pretreatment with E2 in a model of neonatal hippocampal injury obtained by trimethyltin (TMT) administration, characterized by neuronal loss in CA1 and CA3 subfields and astroglial and microglial activation. At post-natal days (P)5 and P6 animals received E2 administration (0.2 mg/kg/die i.p.) or vehicle. At P7 they received a single dose of TMT (6.5 mg/kg i.p.) and were sacrificed 72 h (P10) or 7 days after TMT treatment (P14). Our findings indicate that pretreatment with E2 exerts a protective effect against hippocampal damage induced by TMT administration early in development, reducing the extent of neuronal death in the CA1 subfield, inducing the activation of genes involved in neuroprotection, lowering the neuroinflammatory response and restoring neuropeptide Y- and parvalbumin- expression, which is impaired in the early phases of TMT-induced damage. Our data support the efficacy of estrogen-based neuroprotective approaches to counteract early occurring hippocampal damage in the developing hippocampus.</p>},
  articleno    = {385},
  author       = {Marchese, Elisa and Corvino, Valentina and Di Maria, Valentina and Furno, Alfredo and Giannetti, Stefano and Cesari, Eleonora and Lulli, Paola and Michetti, Fabrizio and Geloso, Maria Concetta},
  issn         = {1662-5102},
  keyword      = {Estrogen,Hippocampus,Neuroinflammation,Neuroprotection,Post-natal development,Trimethyltin},
  language     = {eng},
  month        = {10},
  publisher    = {Frontiers},
  series       = {Frontiers in Cellular Neuroscience},
  title        = {The neuroprotective effects of 17β-estradiol pretreatment in a model of neonatal hippocampal injury induced by trimethyltin},
  url          = {http://dx.doi.org/10.3389/fncel.2018.00385},
  volume       = {12},
  year         = {2018},
}