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Book ChapterDOI

Interactions between noradrenergic and cholinergic systems in the brain

TLDR
It is concluded that there exists a noradrenergic-cholinergic (muscarinic) interaction in the central nervous system which is involved in the control of motor activity.
Abstract
Catalepsy produced by the cholinergic (ACh) agonists, arecoline and pilocarpine, was blocked in rats in which the ascending noradrenergic (NA) projections had been selectively destroyed by intracerebral injections of 6-hydroxydopamine (6-OHDA). The same lesions potentiated the motor stimulant effects of the anticholinergic drugs, scopolamine and atropine. It is concluded that there exists a noradrenergic-cholinergic (muscarinic) interaction in the central nervous system which is involved in the control of motor activity.

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References
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Journal ArticleDOI

Iontophoretic application of opiates to the locus coeruleus.

TL;DR: It is concluded that neuronal sensitivity to opiates has a high positive correlation with autoradiographically determined opiate receptor sites, and this sensitivity to Opiates is blocked by opiate antagonists and is stereospecific in nature.
Journal ArticleDOI

Ascending catecholamine pathways and amphetamine-induced locomotor activity: Importance of dopamine and apparent non-involvement of norepinephrine

TL;DR: Data are consistent with the view that ascending DA projections are a critical substrate for amphetamine-induced hyperkinesia and suggest that ascending NE systems do not play a role in this response.
Journal ArticleDOI

Sleep cycle control and cholinergic mechanisms: Differential effects of carbachol injections at pontine brain stem sites

TL;DR: The results support the hypothesis that cholinergic mechanisms of the pontine tegmentum are involved in desynchronized sleep generation.
Journal ArticleDOI

Catecholamines released from cerebral cortex in the cat; decrease during sensory stimulation.

TL;DR: It is proposed that ACh may regulate CA release at presynaptic CA terminals in the cortex as it does in the periphery and a marked increase in CA release observed on perfusing with nicotine or atropine is consistent with this hypothesis.
Journal ArticleDOI

Neurotransmitter metabolites in the cerebrospinal fluid of man following physostigmine.

TL;DR: In this paper, a 3.0 mg dose of physostigmine or normal saline was given intravenously to 23 normal subjects who had been treated with probenecid.
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