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The usefulness of exogenous nicotine as a factor in the induction of morphogenesis in a tobacco tissue culture medium has been demonstrated. Nicotiana rustica callus cell cultures were grown on a modified Murashige and Skoog medium with 2 mg/l indoleacetic acid (IAA) and 0.2 mg/l kinetin (MMS). Root morphogenesis was induced in roller tube callus cell cultures and solid callus cell cultures grown on MMS without kinetin supplemented with 10-100 mg/l nicotine. Optimal nicotine concentration for root induction was 50 mg/l. Other tests using varying combinations of IAA, kinetin and nicotine produced no obvious morphogenesis, although some changes in the amount of callus growth and endogenous protein concentration did correlate with nicotine concentration relative to the presence of IAA and/or kinetin. In liquid MMS medium, 14C-nicotine was primarily incorporated into the protein fraction of cultured cells while primarily incorporated into the cell wall and/or cell membrane fraction of cells cultured on MMS without kinetin in the medium. In MMS without IAA and MMS without both IAA and kinetin, there was incorporation, but to a lesser extent in both the protein and the cell wall and/or cell membrane fractions. [ABSTRACT FROM AUTHOR]

This study investigates historical and on-going changes in the social control of cigarette smoking and emphasizes the moral, political, organizational. and economic forces which have influenced changes in smoking behavior. Social controls have ranged from a complete ban on cigarette smoking in 14 states at the turn of the century, to the post World War II period when smoking was an established part of the American scene, to the various federal and administrative regulations of today. Two measures of per capita consumption of cigarettes over the past decade have fluctuated widely in accordance with the history of that period. Although health considerations have influenced consumption patterns, data collected by the Federal Government show that moral considerations are probably more important, and that today many cigarette smokers label themselves as deviant. The future bodes greater control over the sale, advertising, and consumption of cigarettes, although prohibition of adult smoking is unlikely. [ABSTRACT FROM AUTHOR]

This study investigated the stimulus property of nicotine in the rat. The primary objectives of the study were 1. to determine the time course of the nicotine stimulus and its relationship to brain levels of the drug and 2. to determine whether the nicotine stimulus is dependent upon the integrity of specific neurotransmitter systems. A lever choice discrimination was used. After injection of nicotine, depression of one lever in an operant test chamber resulted in food reinforcement according to a variable interval schedule of 15 sec. When saline was administered, the opposite lever was reinforced. A high degree of discriminated responding was observed when either 400 Μg/kg or 200 Μg/kg of nicotine was used as a discriminative stimulus. The degree of discrimination decreased as the length of the time period between the injection of nicotine and the test of discrimination was increased. This decline in discrimination was similar to the decline in brain levels of nicotine suggesting that nicotine discrimination is directly related to the concentration of nicotine in the brain. Atropine, mecamylamine, dibenamine, propranolol and α-methyl-para-tyrosine (AMPT) were all tested, in a range of doses, for effects upon nicotine discrimination. Of these, only mecamylamine antagonized the nicotine stimulus. These results indicate that the stimulus effect of nicotine is mediated specifically through nicotinic-cholinergic receptors and not muscarinic-cholinergic or adrenergic receptors. [ABSTRACT FROM AUTHOR]

The effects of nicotine and caffeine on the long-term store of memory in mice were determined for a wide range of dosages. Male F mice (C57BL/6J×DBA/ 2J) were given two trials in an appetitive maze 24 h apart. Twenty-four hours after the second trial each animal was given the first of five daily injections of one of the dosages being tested. Beginning 48 h after the last injection, animals received one trial per day until a learning criterion was reached. Both nicotine and caffeine produced a dose-dependent disruption of performance in the trials following the injection series. In contrast, nicotine produced facilitation of performance in animals given a series of injections in the absence of previous training, and caffeine produced a strong trend in this direction. It was concluded that these drugs produced disruption of the long-term store of memory for the initial training and proactive facilitation of maze learning. The existence of separate and opposing effects of these drugs on different aspects of learning and memory was discussed. [ABSTRACT FROM AUTHOR]

The comparative effects of three doses of nicotine (0.075, 0.15 and 0.3 mg/kg) were measured on the shuttlebox behavior of highly trained guinea pigs, using 50-trial sessions and a 15 sec CS-US interval. It was found that nicotine counteracted the characteristic intra-session performance decrement seen with this species and, in addition, that the various doses of nicotine could be differentiated from each other and the control (physiological saline) in this test. These results were obtained through the measurement of response latencies and the recording of intertriai responses which, for the purposes and conditions of this and future studies of this type, were shown to be more effective parameters than the measurement of avoidance frequency alone. [ABSTRACT FROM AUTHOR]

Rats which had been chronically injected with nicotine or with saline during avoidance training were observed during subsequent avoidance experiments. Among those trained and tested on an unsignalled schedule lever-holding and crouching were frequent and the stimulant effects of nicotine, though consistent, were small. When a warning signal preceded each shock or a feedback signal followed each response lever-holding and crouching were reduced. In these experiments the rats tested with saline were inactive but they tended to lie down rather than crouch during their periods of immobility. Nicotine-treated rats in the signalled experiments were active with high levels of sniffing and grooming behaviour. It is suggested that the lever-holding and crouching in the unsignalled experiment were both aspects of freezing behaviour. [ABSTRACT FROM AUTHOR]

Three tobacco cigarettes with known content of nicotine and one lettuce-leaf cigarette were smoked by 24 young habitual smokers, at different times of day and fixed rates of smoking. Changes in various psychophysiological parameters were automatically recorded during the 60 min which followed smoking. Heart rate and forearm blood flow increases were found to be dose dependent, the latter occurring only after smoking at the fast rate and their duration simultaneous to the presence of active nicotine in the organism. Skin vasoconstriction, as measured by decreases in temperature showed itself more reactive to environmental stimuli than to drug effects. Significant increases in skin conductance levels lasting throughout the experimental session occurred immediately after smoking, although not related to drug effects. Diphasic effects of nicotine were, however, obtained with the two largest doses, at different times of day. This finding is discussed in relation to possible 'unspecific' nicotine effects upon a preexisting level of 'activation'. Nicotine did not influence subjective time estimates. However, a specific pattern of responses occurred. This is discussed in terms of 'disruption' of the timing task and a gradual re-organization towards pre-smoking estimates. The value of psychophysiological indices in relation to drugs of habitual use is questioned. [ABSTRACT FROM AUTHOR]

In experimentally naive rats, nicotine reduced spontaneous locomotor activity in a dose-related manner. After a single pretreatment with nicotine, acute tolerance developed; this was shown by a shift of the dose-response curve, such that the dose of nicotine required to produce a given decrement in activity was multiplied by a factor of about 2.4. In a second experiment, a range of doses of nicotine was found to induce tolerance, but the dose inducing the maximum degree of tolerance was rather critical. The results demonstrated the importance of using a range of pretreatment and challenge doses when assessing tolerance to nicotine. However, frequently repeated doses were not necessary, since tolerance developed when nicotine was administered to rats only once in every 3 days. In terms of tolerance liability in rats, it seems that nicotine is not discriminable from other drugs upon which dependence can be established. [ABSTRACT FROM AUTHOR]

Rats were trained to choose between the side compartments of a three-chambered shock-escape apparatus according to whether they were injected with nicotine or saline. Half of the rats learned to discriminate between 0.4 mg/kg nicotine and saline administered subcutaneously, whereas the other half learned to differentiate between 644 ng nicotine or saline administered intraventricularly. The rats trained by the subcutaneous route of administration had the ability to discriminate between nicotine and saline given intraventricularly and the rats trained by the intraventricular route could differentiate when the two substances were injected subcutaneously. This transfer of state-dependent control of discriminative behaviour between subcutaneously and intraventricularly administered nicotine and saline is presented as evidence for the central origin of the nicotine-produced interoceptive cue. [ABSTRACT FROM AUTHOR]

The effects in squirrel monkeys of nicotine, d-amphetamine, caffeine and dimethylheptyl tetrahydrocannabinol have been examined in three standard behavioral procedures: Fixed Interval, Fixed Ratio and Continuous Shock Avoidance, and two procedures developed to test neuromuscular performance: Physical Activity and Steadiness. Nicotine increased responding in the first half of Fixed Intervals and in Continuous Avoidance; d-amphetamine increased responding under all procedures except Physical Activity; caffeine increased responding under all procedures except Fixed Ratio and DMHP increased responding under all procedures except Continuous Avoidance, where responding was reduced. Nicotine and d-amphetamine caused disruption in the Physical Activity procedure. Thus the different procedures revealed different aspects of the behavioral effects of the drugs. Findings are consistent with interpretation that it is the temporal pattern of the responding under the different procedures that is the dominant factor in determining the behavioral effects of the drugs. [ABSTRACT FROM AUTHOR]

Chewing gum containing nicotine or placebo was given to smokers attending an anti-smoking clinic. During a one week double-blind study subjects receiving nicotine smoked less and chewed less gum than those receiving placebo. The difference in tobacco consumption between the two treatment groups was most apparent among previous heavy smokers. During a 6 month follow-up phase all subjects were offered nicotine-containing chewing gum; the number of nonsmokers then remained fairly constant in the 'initial-nicotine group' while it increased in the 'initial-placebo group'. [ABSTRACT FROM AUTHOR]

The nicotine supply that a smoker obtains from tobacco was considered a major contributing factor for establishing and continuing the smoking habit. The idea that nicotine exerts pharmacological effects which might be strived for by the smoker gains support from reports in the literature both of animal experiments and observations in humans. Hence, it was thought that smoking withdrawal would be more easy if the ex-smoker can supply himself with suitable doses of nicotine while avoiding the dangers of tar and carbon monoxide in the smoke. A chewing gum containing nicotine bound to an ion exchanger was deviced to be used for smoking withdrawal. The advantage of this preparation are that it allows administration in a convenient way of nicotine ad libitum, it precludes intoxication of the preparation if swallowed and it allows reducing the nicotine content for withdrawal purposes while keeping other properties unchanged. The preparation is now undergoing clinical trials. [ABSTRACT FROM AUTHOR]

A Mood Adjective Check List and an 'activation' scale were used to measure subjective reports on mood changes in 24 male habitual smokers before and after smoking cigarettes with known content of nicotine, at different times of day and rates of puffing. Ratings on 'pleasantness' were dose related. 'Aggression' and 'anxiety' showed effects attributable to circadian influence and slight decreases in both factors occurred after smoking the highest nicotine cigarette. The MACL scores were greatly affected by the experimental procedure. Levels of 'inner tension' were found related to the nicotine inhaled. The heuristic value of the concept of 'activation' in these studies is suggested. [ABSTRACT FROM AUTHOR]

Various smoking parameters were studied in 24 habitual smokers smoking cigarettes with known content of nicotine at fixed rates of puffing and times of day. Heart rate and skin temperature were recorded simultaneously. Doses of nicotine inhaled were estimated. Nicotine intake was seen to be closely related to puff length and rate. This occured, however, only when smoking in the afternoon. These findings are discussed in relation to differences in self-reported mood and 'activation' changes at different times of day. Increases in heart rate were found to be dependent on the drug intake. Consistent decreases in skin temperature were observed during the smoking period, although not related to possible drug effects. The usefulness of this variable as an index of nicotine induced vasoconstriction is discussed. [ABSTRACT FROM AUTHOR]

The effects of nicotine, lobeline, anabasine, cytisine, coniine, sparteine, piperidine, acetylcholine, tetramethylammonium (TMA) and dexamphet-amine, given as i.a. bolus injections, were studied in the cat superior cervical ganglion (SCG) in situ and compared with those of (DMPP) 1,1-dimethyl-4-phenylpiperazinium described in a preceding paper. Two main events are thought to determine the ganglionic response to these agents. A non-selective conductance increase of the ganglion cells by stimulation of nicotinic receptors is responsible for depolarization, firing, facilitation of ganglionic transmission and depolarization block. The accumulation of Na resulting from the altered conductance activates an electrogenic Na- pump which tends to increase the membrane potential and causes a delayed unspecific depression of ganglionic excitability. After agents with a brief agonistic action (acetylcholine, DMPP, TMA), the two mechanisms lead to a distinct biphasic effect on ganglionic polarity (initial depolarization, later hyperpolarization) and transmission (early and later block); with the nicotinic agonists of long duration of action the effect of the electrogenic Na-pump was obscured by the long-lasting activation of nicotinic receptors and was usually revealed only by special pharmacological procedures. An additional preganglionic depression of transmitter release is very likely. A desensitization of nicotinic receptors occurred after high single or repeated doses of nicotine, resulting in a selective unsurmountable block. A competitive block of nicotinic receptors occurred after coniine. Local anaesthetic properties of lobeline and dexamphetamine interfered with the two main events when high doses were given. The only effect of sparteine was to produce a short-lasting hexamethonium-like block of transmission. [ABSTRACT FROM AUTHOR]

Evidence is presented to show that nicotine causes desensitization of certain cells of the snail brain. On cholinoceptive cells where the action of nicotine was excitatory (D-cells), nicotine (10 to 10 M) caused a dose-dependent depolarization and a decrease in input resistance. Firing rate was increased in pacemaker cells. On cholinoceptive cells where the action of nicotine was inhibitory (H-cells), nicotine (10 to 10 M) caused a dose-dependent hyperpolarization and a decrease in input resistance. Firing rate was decreased in pacemaker cells. Both the excitatory and inhibitory effects of nicotine were blocked by d-tubocurarine (10 to 10 M) or atropine (10 to 10 M). Hexamethonium (10 M) reduced the response to nicotine on D-cells but not on H-cells. The membrane potential of both D- and H-type cells returned to control in the presence of nicotine. The duration of the nicotine-induced depolarization of cell V7 was 15±0.8 min ( n=10). The duration of the hyperpolarization of cell V5 was 5±0.7 min ( n=4). The duration of the nicotine-induced hyperpolarization of H cells was consistently shorter than the duration of the nicotine-induced depolarization of D cells. The time course of changes in input resistance and firing rate paralleled the time course of changes in membrane potential in both cell types. The duration of the nicotine-induced change in membrane potential, input resistance of firing rate was not related to the concentration of nicotine. Similarly, the duration of the depolarization caused by acetylcholine, carbachol, lobeline or DMPP was not related to the drug concentration. At the time of repolarization after nicotine, the application of a second dose of nicotine had no effect or caused a depolarization that was low in amplitude and brief in duration. d-Tubocurarine (10 to 10 M) reduced the amplitude of the nicotine-induced change in membrane potential but did not affect the duration. Increasing the extracellular calcium concentration from 7 mM to 14 mM decreased the duration of the nicotine-induced changes. Also, increasing the pH from 8.0 to 10.0 decreased the duration. Elevating the extracellular magnesium concentration from 4 mM to 20 mM blocked spontaneous e.p.s.p.'s, i.p.s.p.'s and prevented orthodromic stimulation. In elevated magnesium, nicotine caused a depolarization-repolarization sequence similar to that in normal maguesium. It differed in that the amplitude of the depolarization was decreased and the duration increased. The results indicate that the cholinergic receptors of snail neurons closely resemble the cholinergic receptors of frog sartorius muscle. [ABSTRACT FROM AUTHOR]

Experiments have shown that salivary gland extracts from marine snail Neptunea antiqua contain an agent with muscarine-like actions; in paper chromatograms the active substance behaved like neurine. In the present investigation a comparison was made between gland extracts and neurine on different biological test objects. Experiments show that the extract of the salivary glands of Neptunea antiqua possesses both muscarinic and nicotinic actions. Experiments suggests that the active agent of the extracts is identical with neurine or a closely related compound. If so the gland should contain as much as about 25 mg of neurine per gram of tissue.

The rate of synthesis of nicotinic acid by partially purified cell extracts of Clostridium butylicum was increased when the substrates L-aspartate and formate were replaced by N-formyl- L-aspartate. Aminopterin (0.2 mM) inhibited the synthesis from L-aspartate and formate, but not from N-formyl-L-aspartate. N-Formyl-D-aspartate did not support the synthesis of nicotinic acid. In the presence of aminopterin, radioactivity from 14C-labelled N-formyl-aspartate was incorporated into nicotinic acid by partially purified cell extracts with only low dilution of the molar specific radioactivity. The pattern of labeling in the synthesised nicotinic acid showed that C-2, 3, 7, and 6 of the nicotinic acid were derived from C-2, 3, 4 and the formyl carbon of N-formyl-aspartic acid. Partially purified extracts of Cl. butylicum synthesised N-formyl-aspartic acid from aspartate and formate and this formylation was inhibited by 0.2 mM aminopterin. [ABSTRACT FROM AUTHOR]

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Clinical surveys and biopsy studies demonstrated a close correlation among reverse smoking, nicotine stomatitis, and carcinoma of the palate. [ABSTRACT FROM AUTHOR]

Antagonists of nicotine have been used in an attempt to resolve the continuing controversy about the role of nicotine as the primary reinforcer in cigarette smoking. Mecamylamine, an antagonist which readily penetrates to the central nervous system, increased the rate of cigarette smoking by about 30% in laboratory tests; this was accompanied by reduced blood pressure, impaired performance of a digit symbol substitution test, improved hand steadiness, and by dysphoria. The increased smoking may be regarded as self-titration with nicotine, an interpretation which receives some support from results obtained with pentolinium, an antagonist with predominantly peripheral actions. In the doses used, pentolinium did not affect smoking rate, blood pressure, or hand steadiness, but it impaired digit symbol performance and induced dysphoria. The different results with mecamylamine and pentolinium support previous evidence that the action of nicotine in the central nervous system has a small but clearly demonstrable role as a primary reinforcer of the smoking habit. [ABSTRACT FROM AUTHOR]

Performance in tasks on visual simple- and choice-reaction time was studied in six healthy habitual smokers. Results from a non-smoking condition, and a condition in which each subject smoked four cigarettes, indicated that smoking had a beneficial effect on performance efficiency in both tasks: (a) simple-reaction time increased over time in the non-smoking condition, but remained at the same level in the smoking condition, and (b) choice-reaction time increased slightly in the non-smoking condition, and decreased in the smoking condition. The difference between conditions was statistically significant for simple-reaction time. Hand steadiness was impaired by smoking. Heart rate and systolic pressure increased in the smoking condition, while catecholamine secretion remained relatively unaffected by smoking. Self-estimates of wakefulness and mood showed that smoking was judged to have favourable effects. [ABSTRACT FROM AUTHOR]

Rats were trained to enter one arm of a T-maze after the subcutaneous administration of 0.4 mg/kg and to enter the opposite arm following the injection of an equal volume of saline. Administration of 0.4 mg/kg nicotine isomethonium iodide hydroiodide, 0.4-10.0 mg/kg lobeline sulfate, 2.0 and 4.0 mg/kg d-amphetamine sulfate and 0.25-2.0 mg/kg arecoline hydrobromide produced responses which resembled the established saline effect. Pretreatment with 10.0 mg/kg lobeline had no significant effect on the nicotine-cued response. The inability of these structurally and/or functionally similar drugs to produce a nicotine-like discriminative effect is discussed. [ABSTRACT FROM AUTHOR]

Atropine, when given to rats shortly before acquisition of a conditioned avoidance response, increases the number of correct responses both in that session and in a retention session performed 5 days later; when the drug is given at a longer pre-trial interval, it has, instead, a depressant action. The depressant action is not observed when the performance of a previously well established conditioned response is measured, instead of the acquisition of a new one. Furthermore, the depressant action does not seem to interfere with the previously reported enhancing action of post-trial atropine on memory consolidation. It does, however, block the enhancing effects of nicotine on learning. The stimulant effect of atropine at short pre-trial intervals is mimicked by N-methyl-atropine at moderate doses; the depressant effect of atropine is shared by high doses of the N-methylated analog. The effects of N-methyl-atropine are not time-dependent, as those of the parent compound. [ABSTRACT FROM AUTHOR]

Rats were trained to make a specific behavioral response in a T-maze apparatus conditional upon whether they were injected with 0.4 mg/kg nicotine or saline. Depletion of brain levels of 5-hydroxytryptamine by orally administered para-chlorophenylalanine had no significant effect on the rats' ability to discriminate nicotine. However, both insoluble alpha-methyl-p-tyrosine and its ester, at intraperitoneal doses of 90 and 135 mg/kg, respectively, significantly decreased discrimination of nicotine at 180 and 270 min post-administration. At these doses and times, saline discrimination was not altered. The experimental evidence indicates that nicotine's CNS cueing effect is mediated by norepinephrine, and this is discussed in light of the Burn and Rand hypothesis. It is proposed that, nicotine may act on a specific nicotine-sensitive cholinergic receptor in the CNS, which causes release of norepinephrine which, in turn, produces the interoceptive cueing effect that enables the rats to make the appropriate behavioral response. [ABSTRACT FROM AUTHOR]

One lettuce-leaf and three tobacco cigarettes with different nicotine content were smoked by 24 habitual smokers in the course of 4 successive sessions. Their previous smoking habits were found to be significantly related to their preferences for the various cigarettes. Whilst the heavy smokers (>10 cigarettes per day) preferred only the tobacco cigarettes and strongly disliked the lettuce-leaf, light smokers disliked mostly the highest nicotine cigarette. These ratings were also related to differences in the nicotine intake. It is suggested that these findings support the importance of nicotine in the smoking habit, although other factors may be related to the likableness of tobacco smoking. The relevance of this type of study is discussed. [ABSTRACT FROM AUTHOR]

A series of experiments were conducted to determine whether nicotine facilitates avoidance acquisition by enhancing consolidation or merely by stimulating performance. Sprague-Dawley albino rats were trained for 15 one-hour sessions in a discriminated leverpress avoidance situation with buzzer as a conditioned stimulus. More rats receiving nicotine, 0.4 mg/kg, i.p. immediately before each one-hour daily session (presession) reached a preset learning criterion than did saline controls, and rats receiving 0.1 mg/kg of nicotine performed better than controls but not as well as those receiving the higher nicotine dose. Rats given similar doses of quaternary nicotine bismethiodide in an identical presession experiment did not learn more proficiently than controls. Other groups of rats were given four doses of nicotine in photocell activity cages and the doses of nicotine which facilitated avoidance acquisition actually depressed spontaneous motor activity. Later studies in which rats were given 0.1 and 0.4 mg/kg nicotine or saline i.p. immediately after each session (postsession) showed that the drug also facilitates avoidance acquisition by this method; however, only the lower dose produced significant facilitation in this instance. Finally, rats were again trained with precession nicotine, but saline was substituted for nicotine beginning on session 16. No drug dissociation effect was seen. Thus the results of these studies strongly suggest that small doses of nicotine permanently facilitate the consolidating neural memory trace and do not enhance avoidance acquisition merely by stimulating performance. [ABSTRACT FROM AUTHOR]

Sustained performance in a visual reaction time test was examined in 12 moderate smokers. In a control condition without smoking, efficiency decreased over time. In a, condition, where 3 cigarettes were smoked at 20-min intervals, the subjects were able to maintain their initial level of performance throughout the session, mean reaction times being significantly shorter in the smoking than in the control condition. Smoking produced a significant increase in adrenaline excretion and heart rate. [ABSTRACT FROM AUTHOR]

dl-amphetamine sulphate (2 mg/kg) and nicotine (0.2 mg/kg) showed a facilitatory action on the acquisition of a conditioned response in a shuttle-box by rats and this was reversed by pretreatment with α-MT (30 mg/kg). Pretreatment with dibenamine (10 mg/kg) impaired the action either of amphetamine or nicotine. Nethalide (5-10 mg/kg) exerted a partial protection on the depressant effect produced by the interaction between dibenamine and nicotine. Animals treated with α-MT (30 mg/kg) and kept in the cold (4-6° C for 3 h) also showed a depressed learning capacity. dl-Dopa (200 mg/kg) provided a partial protection on the depressive effects caused by the interaction of α-MT with amphetamine, nicotine or cold. It is suggested that the facilitatory learning action of amphetamine and nicotine involves a common adrenergic mechanism. The depressant effects of amphetamine, nicotine or cold after α-MT treatment are attributed to depletion of 'functional pools' of catecholamines. [ABSTRACT FROM AUTHOR]

Hungry rats were trained on a discrimination task in order to obtain food rewards. During each experimental session, discrete stimuli of 1 min duration were delivered through a small speaker in the experimental chamber at random intervals on the average of once every 2 min. Lever responses in the presence of a light and tone were correct and produced food rewards. Lever responses in the presence of the light stimulus were incorrect and were punished by total inactivation of the experimental chamber. Rats were selected for this experiment based on their inability to acquire the discrimination task even after six months of training. Administration of nicotine, lobeline, chlordiazepoxide and meprobamate produced an improvement in discrimination performance through a reduction of responses to incorrect stimuli. Caffeine and nicotine monomethiodide, the quaternary salt of nicotine, were without effect on the discrimination. [ABSTRACT FROM AUTHOR]

9 subjects were given cigarettes to smoke containing 3 different amounts of nicotine. It was found that the larger the content of nicotine in the cigarettes offered the smaller was the number smoked during the 8-h period. A linear relationship between nicotine content and time to smoke a single cigaretts was found such that the more nicotine there was in a cigarette the longer a subject took to smoke it. [ABSTRACT FROM AUTHOR]

Chronic administration of nicotine (0.5 mg/kg, subcutaneously, 3 to 5 times a day for 6 weeks) accelerated the rate of disappearance of intraventricularly administered H-noradrenaline from rat brain. This was associated with normal levels of H-normetanephrine suggesting an increase in intraneuronal deamination. The rate constant of amine decline ( k) in animals chronically treated with nicotine was significantly greater than that of controls, while the steady state level of brain noradrenaline was about equal in both groups of rats. Amphetamine, reserpine, acetylcholine, histamine, pheniprazine, pargyline, and nicotine affected the catecholamine levels in the rat brain treated with nicotine to the same degree as they did in the controls. It is concluded that chronic administration of nicotine may increase noradrenaline turnover in the brain and possibly increase the deamination of this amine. [ABSTRACT FROM AUTHOR]

The swimming endurance of rats in a water tub was measured until the animals submerged for two seconds under the water surface. The total alkaloid fraction extracted from cigarette smoke produced deterioration of performance in doses of 0.05 to 0.2 mg/kg, whereas pure nicotine (0.1 and 0.2 mg/kg), as well as nicotine pretreated analogously to the extraction process of the total alkaloids produced performance improvements. [ABSTRACT FROM AUTHOR]

The effect of nicotine and total alkaloids extracted from smoke on the avoidance behavior of rats under extinction procedure has been measured in an experiment extended over a period of three months. There was no significant difference between the two substances, with both inhibiting the extinction of avoidance response to approximately the same degree. Significance against the control was achieved with all treatments, the effect being significantly greater with the dose of 0.2 mg/kg than with the two doses of 0.1 or 0.05 mg/kg. [ABSTRACT FROM AUTHOR]

Pre- and post-trial application of 0.15 mg/kg nicotine had, quantitatively and qualitatively, a very similar effect on the Hebb-Williams-test performance of rats. The performance of both treated groups, was for some of the problems of the second half of the test (composed of 12 problems), better than that of the control group. This result suggests a beneficial effect of nicotine on higher integrative functions. The irregularity of the effect from problem to problem of the test was discussed as a consequence of the structural differences between the problems of the test. [ABSTRACT FROM AUTHOR]

Measures of smoking rate and psychological effects of cigarettes with varying nicotine content were made in 15 subjects. While subjects did perceive differences in strength and quality of the experimental lettuce cigarettes as compared to their own brands, their smoking rates did not decrease differentially over the nicotine gradient. The decrement in smoking due to the experimental cigarettes persisted when subjects resumed smoking their own cigarettes. However, the smoking that did occur in the absence of both tobacco and nicotine indicates that the habit itself often exhibits functional autonomy from the physiological effects of nicotine. [ABSTRACT FROM AUTHOR]

The effects of nicotine on bar-pressing behaviour in the rat are blocked by mecamylamine. The depressant phase of the effect is blocked by atropine, supporting the conclusion that this depression is mediated by released acetylcholine. The quaternary compounds chlorisondamine and atropine methylnitrate also antagonise the behavioural effects of nicotine but the doses required for this are far in excess of those which are effective peripherally, suggesting that the sites of interaction are central. [ABSTRACT FROM AUTHOR]