Modulation of cortical in vivo acetylcholine release by the basal nuclear complex: role of the pontomesencephalic tegmental area

Rosalia Bertorelli, GianLuigi Forloni, Silvana Consolo

Research output: Contribution to journalArticlepeer-review

Abstract

Acetylcholine (ACh) release in vivo from rat cortices was determined by microdialysis either after injection of drugs into the basal nuclear complex (NBM) or after electrolytic lesion of the pontomesencephalic tegmental nucleus (PPT). Scopolamine (SCOP) (5-10 μg) increased and oxotremorine (10 μg) reduced cortical ACh release, indicating that an inhibitory mechanism operates within the area. The γ-aminobutyric acid (GABA)ergic antagonist, picrotoxin (2.5 μg), by disinhibiting the cholinergic basocortical neurons, induced an increase that was not affected by SCOP. Acute lesion of the cholinergic PPT efferents to NBM raised cortical basal release. Thus, ACh released from the PPT terminals apparently modulates the function of basocortical neurons mainly through a polysynaptic link via GABAergic neurons.

Original languageEnglish
Pages (from-to)353-356
Number of pages4
JournalBrain Research
Volume563
Issue number1-2
DOIs
Publication statusPublished - Nov 1 1991

Keywords

  • Basocortical pathway
  • Microdialysis
  • Oxotremorine
  • Pedunculopontine tegmental nucleus lesion
  • Picrotoxin
  • Scopolamine

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

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