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

Rosalia Bertorelli; GianLuigi Forloni; Silvana Consolo

doi:10.1016/0006-8993(91)91562-F

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

Rosalia Bertorelli, GianLuigi Forloni, Silvana Consolo

Istituto di Ricerche Farmacologiche "Mario Negri"

Research output: Contribution to journal › Article › peer-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 language	English
Pages (from-to)	353-356
Number of pages	4
Journal	Brain Research
Volume	563
Issue number	1-2
DOIs	https://doi.org/10.1016/0006-8993(91)91562-F
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)

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10.1016/0006-8993(91)91562-F

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

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.",

keywords = "Basocortical pathway, Microdialysis, Oxotremorine, Pedunculopontine tegmental nucleus lesion, Picrotoxin, Scopolamine",

author = "Rosalia Bertorelli and GianLuigi Forloni and Silvana Consolo",

year = "1991",

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AU - Bertorelli, Rosalia

AU - Forloni, GianLuigi

AU - Consolo, Silvana

PY - 1991/11/1

Y1 - 1991/11/1

N2 - 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.

AB - 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.

KW - Basocortical pathway

KW - Microdialysis

KW - Oxotremorine

KW - Pedunculopontine tegmental nucleus lesion

KW - Picrotoxin

KW - Scopolamine

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

Abstract

Keywords

ASJC Scopus subject areas

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