The neuroprotective effects of 17β-estradiol pretreatment in a model of neonatal hippocampal injury induced by trimethyltin
(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
- Marchese, Elisa ; Corvino, Valentina ; Di Maria, Valentina LU ; Furno, Alfredo ; Giannetti, Stefano ; Cesari, Eleonora ; Lulli, Paola ; Michetti, Fabrizio and Geloso, Maria Concetta
- organization
- publishing date
- 2018-10-26
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Estrogen, Hippocampus, Neuroinflammation, Neuroprotection, Post-natal development, Trimethyltin
- in
- Frontiers in Cellular Neuroscience
- volume
- 12
- article number
- 385
- publisher
- Frontiers Media S. A.
- external identifiers
-
- pmid:30416427
- 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
- 2024-03-02 13:28:27
@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>}},
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}},
keywords = {{Estrogen; Hippocampus; Neuroinflammation; Neuroprotection; Post-natal development; Trimethyltin}},
language = {{eng}},
month = {{10}},
publisher = {{Frontiers Media S. A.}},
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}},
doi = {{10.3389/fncel.2018.00385}},
volume = {{12}},
year = {{2018}},
}