Depletion of catecholamines reveals inhibitory effects of bromocryptine and lysuride on neostriatal neurones recorded intracellularly in vitro

P. Calabresi, M. Benedetti, N. B. Mercuri, G. Bernardi

Research output: Contribution to journalArticle

Abstract

Intracellular recordings were obtained from slices of striata from naive and catecholamine-depleted rats. Depletion of catecholamines was obtained by: (i) acute treatment with reserpine (5 mg/kg i.p., 12 hr before sacrifice); (ii) chronic treatment with reserpine (2-3 mg/kg i.p. die for 5 days) and (iii) electrolytic lesion of the homolateral substantia nigra. The ergots, bromocryptine and lysuride (0.1-1 μM), D2 dopamine agonists, did not have detectable effects on the striatal cells of naive animals, but produced a dose-dependent decrease of the excitatory synaptic potentials evoked intrastriatally and recorded from slices depleted of DA; this inhibitory effect was not coupled to changes in membrane potential and input resistance. Lysuride was more potent than bromocryptine. In 78% of the cells recorded, these ergots also produced a decrease in the intrinsic membrane excitability. The inhibitory effects of the ergots were antagonized by the D2 antagonist sulpiride (1 μM), but not by the D1 antagonist SCH 23390 (1 μM). It is concluded that treatments causing depletion of catecholamines, by up-regulating striatal D2 receptors, reveal inhibitory effects of bromocryptine and lysuride.

Original languageEnglish
Pages (from-to)579-587
Number of pages9
JournalNeuropharmacology
Volume27
Issue number6
DOIs
Publication statusPublished - 1988

Keywords

  • bromocryptine
  • D receptors
  • lysuride
  • Parkinson
  • reserpine
  • striatum

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Drug Discovery
  • Pharmacology

Fingerprint Dive into the research topics of 'Depletion of catecholamines reveals inhibitory effects of bromocryptine and lysuride on neostriatal neurones recorded intracellularly in vitro'. Together they form a unique fingerprint.

  • Cite this