Modulation of cortical in vivo acetylcholine release by the basal nuclear complex: role of the pontomesencephalic tegmental area.
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 micrograms) increased and oxotremorine (10 micrograms) reduced cortical ACh release, indicating that an inhibitory mechanism operates within the area. The gamma-aminobutyric acid (GABA)ergic antagonist, picrotoxin (2.5 micrograms), 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.
Bertorelli
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Laboratory of Cholinergic Neuropharmacology, Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.
Forloni
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G
Consolo
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S
D000109:Acetylcholine / Q000378:metabolism* / Q000494:pharmacology; D000818:Animals; D001479:Basal Ganglia / Q000502:physiology*; D002540:Cerebral Cortex / Q000378:metabolism*; D004566:Electrodes; D010095:Oxotremorine / Q000494:pharmacology; D011149:Pons / Q000502:physiology; D051381:Rats; D011976:Receptors, Muscarinic / Q000187:drug effects / Q000378:metabolism; D012601:Scopolamine / Q000494:pharmacology; D013194:Staining and Labeling; D013681:Tegmentum Mesencephali / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
D011976:Receptors, Muscarinic; D013779:Tetrodotoxin; D010095:Oxotremorine; D012601:Scopolamine; D000109:Acetylcholine