Differential steroid hormone and neural influences on peptide mRNA levels in CRH cells of the paraventricular nucleus: a hybridization histochemical study in the rat
Abstract
The three major classes of neurons in the paraventricular nucleus (PVH) provide a rich model for studying hormonal and neural influences on multiple neuropeptides expressed in individual cells. A great deal of previous work has examined this problem at the immunohistochemical level, where hormonal and neural influences on peptide levels have been established. In situ hybridization methods were used here to determine whether these effects are accompanied by measurable changes in neuropeptide mRNA levels. In the first series of experiments, the time-course of corticosterone replacement effects on corticotropin-releasing hormone (CRH) mRNA levels in parvicellular neuroendocrine cells of adrenalectomized animals were determined, and a dose-response curve was established. CRH mRNA hybridization remains maximal with plasma levels of steroid up to about 50 ng/ml, then declines sharply between about 60-130 ng/ml, and is just detectable at higher levels. We confirmed that corticosterone decreases vasopressin mRNA levels in this cell group and showed that levels of preproenkephalin mRNA are also decreased, whereas no significant changes in cholecystokinin, beta-preprotachykinin, and angiotensinogen mRNA levels could be detected. Thus, corticosterone decreases some neuropeptide mRNA levels and has no influence on others in this cell group. Tyrosine hydroxylase mRNA hybridization is also unaffected in this part of the nucleus. In a second group of experiments, the cell-type specificity of corticosterone influences was examined. It was found that while the hormone depresses CRH mRNA levels in parvicellular neurons, it increases such levels in PVH neurons with descending projections, in certain magnocellular neurosecretory neurons, and in a part of the central nucleus of the amygdala, whereas no influence was detected in the rostral lateral hypothalamic area. Furthermore, the stimulatory effects of corticosterone have different threshold levels in different cell groups. Thus, in different types of neurons, corticosterone may increase, decrease, or have no influence on CRH mRNA levels. In contrast, while corticosterone depresses vasopressin mRNA levels in parvicellular CRH neurons, it has no obvious effects on vasopressin mRNA levels in magnocellular or descending neurons; as with CRH, the effects of corticosterone on vasopressin mRNA levels are cell-type specific. In a third series of experiments it was shown that glucocorticoid receptor and mineralocorticoid receptor mRNAs are found in all three cell types in the PVH and that corticosterone tends to produce modest increases in mRNA levels for both receptors. Finally, it was shown that unilateral catecholamine-depleting knife cuts do not change mRNA levels for any of the neuropeptides (or steroid hormone receptors) examined here, although dramatic changes in neuropeptide levels themselves have been shown.4+
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“…increases in CRF and AVP mRNA and peptide expression in parvocellular neurosecretory neurons are well documented (Kiss et al., 1984; Sawchenko et al., 1984; Jingami et al., 1985; Wolfson et al., 1985; Kovács et al., 1986; Young et al., 1986a,b; Kovács and Mezey, 1987; Swanson and Simmons, 1989).”
BackgroundEndocannabinoid system, stress and HPA axis
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- Authors
- Swanson, L. W., & Simmons, D. M.
- Affiliations
- Salk Institute for Biological Studies (US)
- ORCID
- Swanson, L. W.
- Venue
- Journal of Comparative Neurology
- Publisher
- Wiley
- Published
- 1989-07-22
- Volume
- 285
- Issue
- 4
- Pages
- 413-435
- ISSN
- 0021-9967 (ISSN-L)
- 1096-9861
- OpenAlex
- W2074442917
- Cited by
- 478
- References
- 135
- Citations by year
- 2025: 3 · 2024: 3 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 6 · 2019: 3 · 2018: 5 · 2017: 4 · 2016: 3 · 2015: 7 · 2014: 4 · 2013: 9 · 2012: 9
- FWCI
- 11.74
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Journal of Comparative Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Diabetes and Digestive and Kidney Diseases (DK2674109)
- National Institute of Neurological Disorders and Stroke (R01NS 16686, R01NS016686)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
- Keywords
- corticosterone, corticotropin-releasing factor, paraventricular nucleus, vasopressin, preproenkephalin, glucocorticoid receptor, mineralocorticoid receptor, cell type specificity, magnocellular neurosecretory neurons, descending projections, central amygdala, lateral hypothalamus, adrenalectomy
- MeSH terms
- Adrenalectomy, Animals, Autoradiography, Corticosterone, Corticotropin-Releasing Hormone, Kinetics, Male, Neurons, Neuropeptides, Nucleic Acid Hybridization, Paraventricular Hypothalamic Nucleus, Rats, Inbred Strains, Receptors, Glucocorticoid, Reference Values, RNA, Messenger, Sulfur Radioisotopes, Tyrosine 3-Monooxygenase, Rats
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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