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 language | English |
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Pages (from-to) | 353-356 |
Number of pages | 4 |
Journal | Brain Research |
Volume | 563 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 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)