Dopaminergic and noradrenergic responses in the hippocampal slice preparation. Evidence for different receptors

M. G. Marciani, P. Calabresi, P. Stanzione, G. Bernardi

Research output: Contribution to journalArticle

Abstract

The effects of iontophoretic applications of dopamine (DA) and noradrenaline (NA) on potentials evoked by the stimulation of the hippocampal slice preparations were investigated. Dopamine, ejected at the soma, produced an increase of the amplitude of the population spike of CA1 pyramidal cells; NA had an excitatory action on some responses, inhibitory on others. The field-excitatory postsynaptic potentials (EPSPs) were unaffected by ejection of DA and NA on the dendritic tree. Domperidone, a dopaminergic antagonist, blocked the increase of the population spike induced by DA, but was unable to antagonize noradrenergic responses. Timolol, a beta-adrenergic antagonist, blocked the excitatory action of NA, but did not modify either the effect of DA or the inhibition induced by NA. Phentolamine, an alpha-antagonist, antagonized only the inhibition induced by NA. These results indicate that DA and NA modulate the activity of hippocampal neurones by interacting on different receptors.

Original languageEnglish
Pages (from-to)303-307
Number of pages5
JournalNeuropharmacology
Volume23
Issue number3
DOIs
Publication statusPublished - 1984

Fingerprint

Norepinephrine
Dopamine
Domperidone
Timolol
Adrenergic beta-Antagonists
Dopamine Antagonists
Pyramidal Cells
Phentolamine
Excitatory Postsynaptic Potentials
Carisoprodol
Evoked Potentials
Population
Neurons

Keywords

  • antagonists
  • dopamine
  • evoked potentials
  • noradrenaline
  • rat hippocampal slices

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Drug Discovery
  • Pharmacology

Cite this

Dopaminergic and noradrenergic responses in the hippocampal slice preparation. Evidence for different receptors. / Marciani, M. G.; Calabresi, P.; Stanzione, P.; Bernardi, G.

In: Neuropharmacology, Vol. 23, No. 3, 1984, p. 303-307.

Research output: Contribution to journalArticle

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