Über die Zentral Erregende Wirkung des Nicotins

Kuschinsky, G.; Hotovy, R

doi:10.1007/bf01778074

Cited by 16 publications

(4 citation statements)

References 2 publications

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“…Tolerance to a depressant action has also been seen in rats lever-pressing for water reward (Domino and Lutz 1973). In the present study, tolerance did not develop to the stimulant action of nicotine, and parallel findings have been obtained from investigations of locomotor activity (Kuschinksy and Hotovy 1943;Morrison and Stephenson 1972;Clarke and Kumar 1982).…”

Section: Discussionsupporting

confidence: 87%

Nicotine does not improve discrimination of brain stimulation reward by rats

Clarke

Kumar

1983

Psychopharmacology

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Rats were trained to shuttle between two selected ("ON") arms of a Y maze, to obtain electrical stimulation of the medial forebrain bundle. Each shuttle response was rewarded with a brief pulse train. Repetitive entries into the same "ON" arm were not rewarded, nor were entries made into the third ("OFF") arm. Every 67s, stimulation was made available from a different pair of arms. Test sessions lasted for 80 min, beginning immediately after SC injection. Undrugged subjects responded faster, and with a greater proportion of rewarded responses, the higher the stimulation current. In non-tolerant rats, nicotine (0-0.4 mg/kg) depressed responding and induced ataxia shortly after injection; from 40 min, nicotine increased low rates of responding but decreased high rates. All these effects were dose-dependent. Mecamylamine (2.0 mg/kg) prevented the initial depressant action. With repeated daily injections of nicotine (0.4 mg/kg), a marked stimulant action emerged which replaced the initial depressant action, and this was dose-dependent. However, responding was increased by nicotine even when brain stimulation was not available ("time-out"). In contrast, an additional "rate-free" index based on discrimination showed that nicotine did not augment the rewarding properties of the brain stimulation.

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Section: Discussionsupporting

confidence: 87%

Nicotine does not improve discrimination of brain stimulation reward by rats

Clarke

Kumar

1983

Psychopharmacology

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“…Rosecrans, 1972), even when residual tolerance to the locomotor depressant action was found (CorfieldSummer & Stolerman, 1978). Equally, tolerance to the locomotor stimulant action of nicotine has not been found (Kuschinsky & Hotovy, 1943;Morrison & Stephenson, 1972;Battig et al, 1976), although this action should also be attenuated by any metabolic tolerance. Some authors have speculated that tolerance to the behavioural depression may be learnt (Stitzer et al, 1970;Domino & Lutz, 1973;Corfield-Sumner & Stolerman, 1978).…”

Section: Discussionmentioning

confidence: 99%

“…Preliminary studies of the time-course of the effects of nicotine (Kuschinsky & Hotovy, 1943;Rosecrans, 1969) suggest that in non-tolerant rats, nicotine may stimulate activity after an initial period of depression. This is consistent with the results of tests of brief duration carried out at different times after injection (e.g.…”

Section: Introductionmentioning

confidence: 99%

The effects of nicotine on locomotor activity in non‐tolerant and tolerant rats

Clarke¹,

Kumar²

1983

British J Pharmacology

424

185

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1Rats were tested for locomotor activity in photocell cages, for 80 min starting immediately after subcutaneous injection of (-)-nicotine bitartrate or 0.9%w/vNaCl solution (saline). In nontolerant subjects, nicotine (0.1 to 0.4 mg/kg base) depressed activity and induced ataxia in the first 20 min, but increased activity later in the session; these actions were dose-dependent. 2 Tolerance was studied by comparing rats given nicotine (0.4 mg/kg s.c.) every day with control rats given saline instead. Each week, every subject was tested once with nicotine (0.4 mg/kg) and once with saline. With daily or even weekly injections of nicotine, the initial depressant action of the drug was replaced by a dose-dependent stimulant action which occurred throughout the session. In these tolerant animals, little ataxia was seen except when a larger dose of 0.8 mg/kg was given. Tolerance to the depressant action of nicotine persisted for at least 3 weeks. 3 In non-tolerant subjects, mecamylamine (0.5, 1.Omg/kgs.c.) prevented the initial depressant action of nicotine (0.4 mg/kg). In tolerant rats, the locomotor stimulant action of nicotine (0.4 mg/kg) was prevented by mecamylamine (0.1, 0.32, 1.0 mg/kg s.c.) in a dose-related way; the quaternary ganglion blocker, hexamethonium (0.2, 1.0, 5.0 mg/kg s.c.) had little or no such effect. Neither mecamylamine nor hexamethonium altered activity when given alone. 4 It is suggested that a few treatments with nicotine can unmask a stimulant action of the drug, probably of central origin, which possibly reflects a stimulation of nicotine receptors.

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“…Nicotine, at low doses, increases overall activity in rats. At higher doses, nicotine initially depresses and then activates ongoing behavior (e.g., Kuschinsky and Hotovy, 1943;Rosecrans, 1969;Morrison and Stephenson, 1972;Stolerman et al, 1973;Battig et al, 1976;Schlatter and Battig, 1979;Michael, 1986, 1992;Jerome and Sandberg, 1987;Clarke et al, 1988;Hakan, 1988;Fung, 1990;Museo and Wise, 1990;Reavill and Stolerman, 1990;Coen, 1991, 1994;O'Neill et al, 1991;Helton et al, 1993;Brioni et al, 1994;Shoaib et al, 1994;Reid et al, 1998;Nadal and Samson, 1999). Tolerance of the depressant effect occurs and, subsequently, the stimulant action of nicotine becomes more pronounced with repeated administration (e.g., Clarke and Kumar, 1983a, b;Weltzl et al, 1988).…”

Section: Nicotine Produces General Activation and Stimulates Ongoing mentioning

confidence: 99%

Nicotine Self-Administration in Animals: A Reevaluation

Dar

Frenk

2002

Addiction Research & Theory

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Nicotine self-administration in animals is often viewed as compelling evidence that nicotine is reinforcing to animals and as corroborating the widely accepted thesis that nicotine is a major cause of smoking. This review examines the studies of nicotine self-administration in animals in the past two decades, focusing on threats to the internal and external validity of these studies and on the extent to which they support the thesis that nicotine is reinforcing in animals. The review shows that nicotine self-administration studies are fraught with severe methodological problems. These include omission of essential controls for general activation and other systemic effects of nicotine, insufficient consideration of secondary reinforcement processes, using food-deprived or confined animals and exclusion of subjects that do not conform to the investigators' preferred behavior. As a result of these systematic flaws, the role of nicotine as a reinforcer in this paradigm has not been established.

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Über die Zentral Erregende Wirkung des Nicotins

Cited by 16 publications

References 2 publications

Nicotine does not improve discrimination of brain stimulation reward by rats

Nicotine does not improve discrimination of brain stimulation reward by rats

The effects of nicotine on locomotor activity in non‐tolerant and tolerant rats

Nicotine Self-Administration in Animals: A Reevaluation

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