Cited by 61Neuroscience and Neuropharmacology ResearchReceptor Mechanisms and SignalingMemory and Neural Mechanisms

Noradrenergic depression of synaptic responses in hippocampus of rat: Evidence for mediation by alpha1-receptors

Mynlieff, M·1988·Neuropharmacology

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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Crossref · 10.1016/0028-3908(88)90148-7

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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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