Alteration in nuclear factor-kappaB pathway and functionality of estrogen via receptors promote neuroinflammation in frontal cortex after 1-Methyl-4-Phenyl-1,2,3,6-tetrahydropyridine treatment
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The MPTP mediated neurodegeneration in substantia nigra has been well studied, but not the status of frontal cortex. The novelty of the present study is to explore the sex difference of frontal cortex during MPTP intoxication and to investigate the role of estrogen and its receptors in presence of glial cells in a time chase experiment; to identify which pathway of NF-kappaB exist to proceed the neuroinflammation; to investigate the estrogen binding with its nuclear or cytosolic receptors and whether any direct relation exists between estrogen receptor (ER) -beta and NF-kappaB molecules p65 and RelB. The progression of neurodegeneration occurred with the association of glial cells and functional (via its nuclear and cytosolic receptors) estrogen level. Both the canonical and/or non canonical pathways of NF-kappaB exist in frontal cortex of both the sexes after MPTP treatment. The homodimeric or heterodimeric form of ER-beta binds with NF-kappaB molecules p65 and RelB differently, but the canonical or non canonical pathways of NF-kappaB molecules could not be stopped or may be promoted. The changes in the molecular and cellular pattern in frontal cortex of both sexes during MPTP intoxication depends on the estrogen function via its nuclear or cytosolic estrogen receptors.
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Testosterone may be converted to estradiol via the aromatase enzyme, which is present in the frontal cortex.
“Testosterone may be converted to estradiol via the aromatase enzyme, which is present in the frontal cortex (Akther et al., 2015; Mitra et al., 2015)”
From Does puberty mark a transition in sensitive periods for plasticity in the associative neocortex? (2017) · cites this paper as Mitra et al., 2015
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- Authors
- Mitra, S., Ghosh, N., Sinha, P., Chakrabarti, N., & Bhattacharyya, A.
- Affiliations
- University of Calcutta (IN)
- Corresponding author
- Bhattacharyya, Arindam
- Venue
- Scientific Reports
- Published
- 2015-09-14
- Volume
- 5
- Issue
- 1
- Pages
- 13949-13949
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC4568517
- OpenAlex
- W2394639973
- Cited by
- 11
- References
- 51
- Citations by year
- 2025: 2 · 2022: 1 · 2020: 2 · 2019: 2 · 2018: 3 · 2016: 1
- FWCI
- 0.71
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Department of Biotechnology, Ministry of Science and Technology, India
- Indian Council of Medical Research (5/8/4-4)
- Council of Scientific and Industrial Research, India (09/028, 09/028 (0896)/2012-EMR-1)
- University Grants Commission
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Keywords
- MPTP, neuroinflammation, frontal cortex, estrogen receptor beta, NF-κB signaling, RelB, NF-κB p65, glial cells, sex differences, neurodegeneration, Parkinson's disease model
- MeSH terms
- Animals, Aromatase, Calcium-Binding Proteins, Enzyme-Linked Immunosorbent Assay, Estrogens, Female, Frontal Lobe, Glial Fibrillary Acidic Protein, Immunohistochemistry, Inflammation, Male, Microfilament Proteins, Neuroglia, Protein Binding, Tamoxifen, Tumor Necrosis Factor-alpha, NF-kappa B, MPTP Poisoning, Estrogen Receptor alpha, Estrogen Receptor beta, Mice, Transcription Factor RelB, Transcription Factor RelA, Transcriptome
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