Effects of glucocorticoids and norepinephrine on the excitability in the hippocampus
Abstract
The CA1 pyramidal neurons in the hippocampus contain a high density of adrenal corticosteroid receptors. By intracellular recording, CA1 neurons in slices from adrenalectomized rats have been found to display a markedly reduced afterhyperpolarization (that is, the hyperpolarizing phase after a brief depolarizing current pulse) when compared with their sham controls. No differences were found for other tested membrane properties. Brief exposure of hippocampal slices from adrenalectomized rats to glucocorticoid agonists, 30 to 90 minutes before recording, greatly enhanced the afterhyperpolarization. In addition, glucocorticoids attenuated the norepinephrine-induced blockade of action potential accommodation in CA1 neurons. The findings indicate that glucocorticoids can reduce transmitter-evoked excitability in the hippocampus, presumably via a receptor-mediated genomic action.
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Stress levels of corticosterone applied for a longer period of time (>20 minutes) increased the magnitude of inhibitory components of electrophysiological activity, such as the afterhyperpolarization, and suppressed the induction of LTP.
“Conversely, stress levels of corticosterone applied for a longer period of time (>20 minutes) increased the magnitude of inhibitory components of electrophysiological activity, such as the afterhyperpolarization (Joëls and de Kloet [233]; Kerr et al. [234]; Joëls and de Kloet [235]; Karst and Joëls [236]), and suppressed the induction of LTP (Pavlides et al. [237]; Rey et al. [238]; Kerr et al. [”
From The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007) · cites this paper as Joëls and de Kloet [233]
Basal levels of CORT are required for the synthesis of epinephrine in the adrenals and for proper norepinephrine signaling.
“CORT plays a role in this immune activation as well because basal levels of CORT are required for the synthesis of E in the adrenals (Wurtman and Axelrod, 1966) and for proper NE signaling (Joels and de Kloet, 1989).”
From The Stressed CNS: When Glucocorticoids Aggravate Inflammation (2009) · cites this paper as Joels and de Kloet, 1989
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References 48 · Cited by 375
- Authors
- Joëls, M., & de Kloet, E. R.
- Affiliations
- Utrecht University (NL)
- ORCID
- Joëls, Marian
- Venue
- Science
- Published
- 1989-09-29
- Volume
- 245
- Issue
- 4925
- Pages
- 1502-1505
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2008213128
- Cited by
- 375
- References
- 48
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 5 · 2022: 5 · 2021: 3 · 2020: 4 · 2019: 9 · 2018: 4 · 2017: 12 · 2016: 7 · 2015: 4 · 2014: 6 · 2013: 11 · 2012: 8
- FWCI
- 7.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- University of Groningen research database (University of Groningen / Centre for Information Technology) (submittedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- glucocorticoids, norepinephrine, hippocampus, CA1 pyramidal neurons, neuronal excitability, afterhyperpolarization, adrenalectomy, corticosteroid receptors
- MeSH terms
- Action Potentials, Adrenalectomy, Animals, Glucocorticoids, Hippocampus, Membrane Potentials, Neurons, Norepinephrine, Rats, In Vitro Techniques
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