The developmental changes of Nav1.1 and Nav1.2 expression in the human hippocampus and temporal lobe
Abstract
Alterations of the genes encoding α1 and α2 subunits of voltage-gated sodium channels (SCN1A, SCN2A) have been reported as causes of various types of epilepsy, most of which occur during the first year of life; as yet, however, the detailed mechanisms are unclear. We suppose that developmental changes of SCN1A and SCN2A in the human brain, which are unknown yet, may play an important role. So here, we studied the developmental changes of their corresponding proteins (Na(v)1.1 and Na(v)1.2) in the human hippocampus and temporal lobe in 28 autopsy cases, which age from 13weeks of gestation (GW) to 63years of age (Y). Using comparative microscopic immunohistochemical (IHC) analysis, we found that Na(v)1.1 and Na(v)1.2 immunoreactivity first appeared at 19GW, simultaneously in the hippocampus and the white matter of temporal lobe. In nearly all age groups, Na(v)1.1 immunoreactivity was weak and relatively homogeneous. In general, Na(v)1.1 immunoreactive (IR) neurons and neurites increased during the late fetal and postnatal periods, reached their peaks 7-9months after birth (M), then decreased and remained stable at a relatively low level during childhood and adulthood. On the other hand, Na(v)1.2 immunoreactivity was strong and heterogeneous. In the hippocampus, Na(v)1.2 IR neurons increased gradually during the late fetal period, reached their peaks at 7-9M, sustained this high level during childhood, and then decreased slightly at adulthood. In the temporal lobe, Na(v)1.2 IR neurons reached a high level during the late fetal period, and maintained that level during subsequent developmental stages; Na(v)1.2 IR neurites also increased to a relatively high level during the late fetal period and continued to increase up to and during adulthood. Using double-staining IHC, we found that Na(v)1.1 and Na(v)1.2 had a relatively high colocalization rate with parvalbumin and showed distinct developmental changes. These findings extend our previous understanding of sodium channels and may help us discover the pathomechanisms of sodium channel-related age-dependent epilepsy.
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Nav1.1, a voltage-gated sodium channel found largely on PV-IN axons, is decreased in a mouse model with amyloid pathology and in AD patients.
“Separately, a voltage-gated sodium channel (Na v 1.1) that is largely found on axons of PV-INs was decreased in a mouse model with amyloid pathology, and in AD patients [24][25][26].”
From Parvalbumin interneuron vulnerability and brain disorders (2021) · cites this paper as [25]
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- Authors
- Wang, W., Takashima, S., Segawa, Y., Itoh, M., Shi, X., Hwang, S.-K., Nabeshima, K., Takeshita, M., & Hirose, S.
- Affiliations
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Fukuoka International University of Health and Welfare (JP)
- Fukuoka University (JP)
- National Center of Neurology and Psychiatry (JP)
- Corresponding author
- Hirose, Shinichi
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2011-05
- Volume
- 1389
- Pages
- 61-70
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W2093258733
- Cited by
- 47
- References
- 31
- Citations by year
- 2026: 1 · 2025: 6 · 2024: 4 · 2023: 4 · 2022: 4 · 2021: 3 · 2020: 4 · 2019: 2 · 2018: 4 · 2017: 3 · 2016: 1 · 2015: 3 · 2014: 1 · 2013: 4 · 2012: 2
- FWCI
- 1.04
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Fukuoka University (19A-6, 21B-5)
- Central Research Institute, Fukuoka University
- Ministry of Education, Culture, Sports, Science and Technology
- Ministry of Health, Labour and Welfare
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Nav1.1, Nav1.2, voltage-gated sodium channels, SCN1A, SCN2A, human brain development, hippocampus, temporal lobe, parvalbumin
- MeSH terms
- Adolescent, Adult, Child, Child, Preschool, Fetus, Hippocampus, Humans, Immunohistochemistry, Infant, Infant, Newborn, Microtubule-Associated Proteins, Middle Aged, Nerve Growth Factors, Temporal Lobe, Young Adult
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