Effects of cholinergic drugs on hypothalamic self-stimulation response rates of dogs

Stark, Paul; Boyd, Eugene S.

doi:10.1152/ajplegacy.1963.205.4.745

Cited by 82 publications

(20 citation statements)

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“…It is very likely that neostigmine, which poorly crosses the bloodbrain barrier, served as an "active placebo." First, this drug has been found to be 2-3 times more potent in the periphery than is physostigmine (11). Also, in our studies, we frequently noted that the peripheral effects of neostigmine, including antagonism of methylscopolamine's effects, bradycardia, perspiration, and muscle fasiculations occurred without accompanying behavioral changes, and that these effects occurred in a higher percentage of neostigmine treated patients than in physostigmine treated patients.…”

Section: Resultsmentioning

confidence: 48%

“…In the study, two types of controls were utilized. First, in 13 of the patients, neostigmine, a cholinesterase inhibitor which does not effectively pass the blood-brain barrier and which is 2-3 times as potent as physostigmine in the periphery, was used as an active placebo (11) instead of physostigmine. Second, the patient and the rating nurse did not know which of a series of injections was placebo and which was active drug.…”

Section: Methodsmentioning

confidence: 99%

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Acetylcholine and Depression*

Janowsky

El-Yousef

Davis

1974

Psychosomatic Medicine

206

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Physostigmine, a cholinesterase inhibitor which increases central acetylcholine levels, has been found in man to decrease manic symptoms, antagonize methylphenidate-induced behavioral activation, and induce severe depression and psychomotor retardation in marijuana intoxicated normals. In the current study, physostigmine was found to increase depressed mood in patients with an affective component to their symptoms (manics, depressives, and schizoaffectives). Schizophrenics without an affective component did not become depressed. After physostigmine administration, all subject groups showed a significant increase in symptoms including lethargy, slowed thoughts, withdrawal, apathy, decreased energy, decreased thoughts, motor retardation, and feeling drained, indicating a state of psychomotor retardation; and all became less cheerful, friendly, and talkative. The above information is compatible with the hypothesis that acetylcholine may be involved in the etiology of affective disorders.

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Section: Resultsmentioning

confidence: 48%

Section: Methodsmentioning

confidence: 99%

Acetylcholine and Depression*

Janowsky

El-Yousef

Davis

1974

Psychosomatic Medicine

206

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“…Results of previous comparisons of behavioral effects of physostigmine and neostigmine have indicated that physostigmine has greater effects on behavior than neostigmine in rats and dogs (Stark and Boyd 1963;Domino and Olds 1968). On the other hand, Wenger (1979) reported that neostigmine decreased food-maintained responding of mice at lower molar doses than physostigmine.…”

Section: Discussionmentioning

confidence: 99%

Central and peripheral muscarinic actions of physostigmine and oxotremorine on avoidance responding of squirrel monkeys

Witkin

1989

Psychopharmacology

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The involvement of central and peripheral muscarinic cholinergic receptors in the behavioral effects of the cholinesterase inhibitor physostigmine was evaluated by comparing the ability of atropine and methylatropine to reverse the effects of physostigmine, the muscarinic agonist oxotremorine, or their quaternary analogs neostigmine and oxotremorine-M. Avoidance behavior was maintained under a schedule in which every lever press postponed delivery of electric shock for 20 s; shock occurred every 5 s in the absence of responding. Cumulative doses of physostigmine or oxotremorine produced dose-related decreases in response rates, and increases in response durations and rates of shock delivery. Similar effects occurred with neostigmine and oxotremorine-M. Methylatropine completely prevented the behavioral and parasympathetic effects of neostigmine and oxotremorine-M without having any behavioral effects of its own. However, methylatropine did not alter the behavioral effects of physostigmine or oxotremorine. Atropine prevented the peripheral manifestations as well as the behavioral effects of physostigmine and oxotremorine even though atropine decreased avoidance responding when given alone. These results suggest that in squirrel monkeys, central and peripheral muscarinic receptors may function in a redundant manner to control agonist-induced decrements in avoidance. When physostigmine or oxotremorine was given in conjunction with atropine, rates of avoidance responding were increased to 180% of control levels. Response rate increases after administration of oxotremorine or physostigmine in monkeys treated with atropine may reflect a non-muscarinic action of atropine, unmasked by the presence of cholinomimetics.

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“…In a separate experiment, nine other subjects were infused with 0.011 mg/kg neostigmine. This dose is approximately equipotent to 0.022 mg/kg physostigmine in its peripheral anticholinesterase effects in dogs (8). It also has a similar LD-50 in rats and mice (The Merck Index, 1983, Merck & Co., Inc., Rahway, NJ).…”

Section: Methodsmentioning

confidence: 99%

Central cholinergic stimulation causes adrenal epinephrine release.

Kennedy¹,

Janowsky²,

Risch³

1984

J. Clin. Invest.

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Abstract. Cholinergic drugs administered into the cerebral ventricles of animals selectively stimulate the adrenal medulla. However, the effects of central cholinergic stimulation on the sympathoadrenal system have not been studied in man. We stimulated central cholinergic activity in man by administering the cholinesterase inhibitor physostigmine to subjects pretreated with peripheral cholinergic blocking agents. A dose of 0.022 mg/kg physostigmine dramatically increased plasma epinephrine levels and slightly increased norepinephrine levels, which is consistent with selective adrenomedullary stimulation. A smaller dose of physostigmine increased epinephrine but did not alter norepinephrine levels. Subjects had increased pulse rates and blood pressures, and felt anxious while they had high plasma epinephrine levels.

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Effects of cholinergic drugs on hypothalamic self-stimulation response rates of dogs

Cited by 82 publications

References 0 publications

Acetylcholine and Depression*

Acetylcholine and Depression*

Central and peripheral muscarinic actions of physostigmine and oxotremorine on avoidance responding of squirrel monkeys

Central cholinergic stimulation causes adrenal epinephrine release.

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