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Noradrenergic enhancement of long-term potentiation at mossy fiber synapses in the hippocampus
Abstract
1. We tested several hypotheses related to the modulation of long-term potentiation (LTP) by norepinephrine (NE) at the mossy fiber synapses in the rat hippocampal slice preparation using extracellular and intracellular recording techniques. 2. NE exerted frequency-dependent effects on mossy fiber synaptic transmission. It had little effect on extracellular population excitatory postsynaptic potentials (pEPSPs) sampled during low-frequency stimulation, whereas it had marked effects on the duration, magnitude, and probability of induction of LTP at these synapses. 3. The beta-adrenoceptor agonist isoproterenol mimicked all of the effects of NE, whereas the beta-adrenoceptor antagonists propranolol and timolol reversibly blocked the induction of LTP, suggesting the effects of NE are mediated by a beta-adrenoceptor and that beta-adrenoceptor activation may be an important constituent for the expression of LTP at these synapses. 4. Frequency-dependent effects of NE and isoproterenol on mossy fiber pEPSPs were also observed in the presence of the gamma-aminobutyric acid (GABA) antagonist, picrotoxin, suggesting that NE can enhance LTP by a mechanism that does not depend on intact inhibition. However, propranolol did not block LTP in these disinhibited slices and did not affect LTP magnitude. 5. The adenylate cyclase activator forskolin augmented pEPSPs sampled during low-frequency stimulation in disinhibited slices and significantly enhanced LTP. Forskolin, however, did not produc…
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“Moreover, neuromodulators can change the induction rules and time course of mossy fiber plasticity [101,102].”
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 [101]
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“For example, high levels of noradrenaline acting at α1- and β-receptors enhance memory consolidation processes in the hippo-campus82,83 and increase the signal/noise ratio in primary sensory cortices84–86.”
From Stress signalling pathways that impair prefrontal cortex structure and function (2009) · cites this paper as [82]
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Metadata
- Authors
- Hopkins, W. F., & Johnston, D.
- Affiliations
- Baylor College of Medicine (US)
- Venue
- Journal of Neurophysiology
- Publisher
- American Physiological Society
- Published
- 1988-02-01
- Volume
- 59
- Issue
- 2
- Pages
- 667-687
- ISSN
- 0022-3077 (ISSN-L)
- 1522-1598
- OpenAlex
- W2403704540
- Cited by
- 310
- References
- 0
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 2 · 2022: 5 · 2021: 5 · 2020: 1 · 2019: 3 · 2018: 4 · 2016: 4 · 2015: 4 · 2014: 8 · 2012: 7
- FWCI
- 5.37
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurophysiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Heart, Lung, and Blood Institute (HL-31164)
- National Institute of Neurological Disorders and Stroke (NS-11535, NS-15772)
- 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
- norepinephrine, long-term potentiation, mossy fiber synapses, hippocampus, beta-adrenergic receptors, isoproterenol, propranolol, timolol, cyclic AMP, forskolin, 8-bromo-cAMP, synaptic transmission, GABAergic inhibition, tetanic stimulation, synaptic plasticity
- MeSH terms
- Animals, Colforsin, Hippocampus, Isoproterenol, Male, Nerve Fibers, Neural Inhibition, Norepinephrine, Picrotoxin, Rats, Inbred Strains, Receptors, Adrenergic, beta, Synapses, Time Factors, 8-Bromo Cyclic Adenosine Monophosphate, Rats
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