The role of serotonin in the development and environmental regulation of type II corticosteroid receptor binding in rat hippocampus
Abstract
Hippocampal concentrations of serotonin (5-HT) increase over the first two weeks of life, and show a peak on day 14. This pattern is very similar to the previously reported developmental changes in hippocampal type II corticosteroid receptor binding. We found that adult animals treated during the first days of life with the 5-HT neurotoxin, 5.7-dihydroxytryptamine, showed reduced hippocampal type II corticosteroid receptor binding. In addition, manipulations that resulted in increased hippocampal type II corticosteroid receptor binding, such as neonatal handling or exogenous thyroid hormone treatment also increased hippocampal 5-HT turnover. Finally, concurrent administration of the 5-HT2 receptor antagonist, ketanserin, blocked the effects of handling on hippocampal type II corticosteroid receptor binding. Taken together with the results of recent in vitro experiments, these data suggest that (a) 5-HT may be involved in the ontogenetic variation in hippocampal type II corticosteroid receptor binding, and (b) that increases in 5-HT activity may mediate the effects of environmental stimulation on hippocampal type II corticosteroid receptor binding.
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Maternal effects on hippocampal GR expression are mediated by increases in hippocampal serotonin turnover and expression of the NGFI-A transcription factor.
“In vivo studies with rat pups or in vitro studies using cultured hippocampal neurons suggest that maternal effects on hippocampal GR expression are mediated by increases in hippocampal serotonin (5-HT) turnover and the expression of the nerve-growth factor-inducible factor-A (NGFI-A) transcription factor.78-82”
From Early life adversity and the epigenetic programming of hypothalamic-pituitary-adrenal function (2014) · cites this paper as [81]
In vivo, the effect on GR is blocked with 5-HT receptor antagonists.
“In vivo, the effect on GR is blocked with 5-HT receptor antagonists.80,81”
From Early life adversity and the epigenetic programming of hypothalamic-pituitary-adrenal function (2014) · cites this paper as [81]
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- Authors
- Mitchell, J. B., Iny, L. J., & Meaney, M. J.
- Affiliations
- Douglas Mental Health University Institute (CA)
- Corresponding author
- Meaney, Michael J.
- ORCID
- Meaney, Michael J.
- Venue
- Developmental Brain Research
- Publisher
- Elsevier BV
- Published
- 1990-09
- Volume
- 55
- Issue
- 2
- Pages
- 231-235
- ISSN
- 0165-3806 (ISSN-L)
- OpenAlex
- W1990088315
- Cited by
- 139
- References
- 2
- Citations by year
- 2025: 1 · 2023: 2 · 2022: 1 · 2020: 1 · 2019: 1 · 2018: 4 · 2017: 4 · 2015: 5 · 2014: 6 · 2013: 7 · 2012: 11
- FWCI
- 2.92
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Developmental Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- serotonin, hippocampus, receptor binding, ontogeny, neonatal handling, thyroid hormones, ketanserin, 5-HT2 receptor, environmental enrichment
- MeSH terms
- Animals, Hippocampus, Hydroxyindoleacetic Acid, Receptors, Glucocorticoid, Serotonin, 5,7-Dihydroxytryptamine, Rats
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