β-Adrenergic receptor signaling and modulation of long-term potentiation in the mammalian hippocampus
Open accessAbstract
Encoding new information in the brain requires changes in synaptic strength. Neuromodulatory transmitters can facilitate synaptic plasticity by modifying the actions and expression of specific signaling cascades, transmitter receptors and their associated signaling complexes, genes, and effector proteins. One critical neuromodulator in the mammalian brain is norepinephrine (NE), which regulates multiple brain functions such as attention, perception, arousal, sleep, learning, and memory. The mammalian hippocampus receives noradrenergic innervation and hippocampal neurons express β-adrenergic receptors, which are known to play important roles in gating the induction of long-lasting forms of synaptic potentiation. These forms of long-term potentiation (LTP) are believed to importantly contribute to long-term storage of spatial and contextual memories in the brain. In this review, we highlight the contributions of noradrenergic signaling in general and β-adrenergic receptors in particular, toward modulating hippocampal LTP. We focus on the roles of NE and β-adrenergic receptors in altering the efficacies of specific signaling molecules such as NMDA and AMPA receptors, protein phosphatases, and translation initiation factors. Also, the roles of β-adrenergic receptors in regulating synaptic “tagging” and “capture” of LTP within synaptic networks of the hippocampus are reviewed. Understanding the molecular and cellular bases of noradrenergic signaling will enrich our grasp of how the brain makes new, enduring memories, and may shed light on credible strategies for improving mental health through treatment of specific disorders linked to perturbed memory processing and dysfunctional noradrenergic synaptic transmission.
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Isoproterenol is a β1 and β2 adrenergic receptor agonist known to activate adenylyl cyclase via Gs proteins.
“we applied 1 μM isoproterenol, a β1 and β2 adrenergic receptor agonist, known to activate AC via Gs proteins (Fig 2D–2K) [52–54].”
From Presynaptic cAMP-PKA-mediated potentiation induces reconfiguration of synaptic vesicle pools and channel-vesicle coupling at hippocampal mossy fiber boutons (2024) · cites this paper as [52]
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- Authors
- O'Dell, T. J., Connor, S. A., Guglietta, R., & Nguyen, P. V.
- Affiliations
- University of Alberta (CA)
- University of California, Los Angeles (US)
- Corresponding author
- Nguyen, Peter V.
- Venue
- Learning & Memory
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2015-08-18
- Volume
- 22
- Issue
- 9
- Pages
- 461-471
- ISSN
- 1072-0502 (ISSN-L)
- 1549-5485
- PMC
- PMC4561407
- OpenAlex
- W1837231696
- Cited by
- 163
- References
- 164
- Citations by year
- 2026: 10 · 2025: 18 · 2024: 13 · 2023: 14 · 2022: 13 · 2021: 19 · 2020: 16 · 2019: 20 · 2018: 17 · 2017: 15 · 2016: 7 · 2015: 1
- Type
- posted content
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- Learning & Memory (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- University of Alberta
- Natural Sciences and Engineering Research Council of Canada
- ARCS Foundation
- Alberta Heritage Foundation
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural dynamics and brain function
- Keywords
- beta-adrenergic receptors, norepinephrine, long-term potentiation, hippocampus, synaptic plasticity, noradrenergic signaling, NMDA receptor, AMPA receptors, protein phosphatase, translation initiation factors, synaptic tagging and capture, memory consolidation, spatial memory, contextual memory
- MeSH terms
- Animals, Hippocampus, Humans, Memory Disorders, Neurons, Receptors, Adrenergic, beta, Long-Term Potentiation
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