Noradrenergic depression of synaptic responses in hippocampus of rat: Evidence for mediation by alpha1-receptors
Abstract
Norepinephrine (NE) has been shown to have a biphasic effect on evoked potentials in the CA1 region of the hippocampus of the rat in vitro, with a beta receptor mediating an increase and an alpha receptor eliciting a decrease in the amplitude of the population spike. The purpose of this study was to use selective alpha-adrenergic agonists and antagonists to determine the subtype of receptor mediating the depressant response of NE. The present investigations demonstrated that the selective alpha 1 agonist, phenylephrine (2-50 microM) elicited a dose-dependent depression of the amplitude of the population spike. Clonidine, a relatively selective alpha 2-agonist, also depressed the amplitude of the population spike, but only at concentrations (10 microM) that were inconsistent with a selective action upon alpha 2-receptors. Another alpha 2-agonist, alpha-methylnorepinephrine (100-400 nM) did not depress the amplitude of the population spike. The depressant effect of NE was antagonized by the nonselective alpha antagonist, phentolamine (0.5-50 microM) and the alpha 1-selective antagonist, prazosin (1 microM), but not by the alpha 2-selective antagonist, idazoxan (1-10 microM). Phentolamine and prazosin antagonized the response to phenylephrine but not to clonidine. The depressant effect of NE was not antagonized by the antagonist of serotonin and dopamine, spiperone (100 nM); conversely, the effect of 8-hydroxy-2-(di-n-propylamine) tetralin (50 microM), a 5-HT1A receptor-selective agonist, which also depresses the amplitude of the population spike, was not antagonized by phentolamine (5 microM).(ABSTRACT TRUNCATED AT 250 WORDS)
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Noradrenaline reduces excitatory synaptic transmission by acting on α-adrenergic receptors.
“Noradrenaline increases the excitability of neurons that express β-adrenergic receptors187–189 and reduces excitatory synaptic transmission by acting on α-adrenergic receptors190,191”
From Mechanisms underlying gain modulation in the cortex (2020) · cites this paper as [191]
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- Authors
- Mynlieff, M.
- Affiliations
- University of Colorado Denver (US)
- Corresponding author
- Mynlieff, M
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 1988-04
- Volume
- 27
- Issue
- 4
- Pages
- 391-398
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W2077413595
- Cited by
- 61
- References
- 24
- Citations by year
- 2023: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2014: 3 · 2012: 2
- FWCI
- 2.96
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Rensselaer Polytechnic Institute
- National Institute on Drug Abuse (DA02702)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- norepinephrine, alpha1-adrenoceptors, alpha2-adrenoceptors, hippocampus, CA1 region, population spike, synaptic depression, phenylephrine, clonidine, prazosin, phentolamine, idazoxan, 5-HT1A receptor
- MeSH terms
- Animals, Evoked Potentials, Hippocampus, Male, Norepinephrine, Rats, Inbred Strains, Receptors, Adrenergic, alpha, Synapses, Rats, In Vitro Techniques
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