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

Clarke, Paul B. S.; Kumar, Ramesh

doi:10.1111/j.1476-5381.1983.tb09398.x

Cited by 424 publications

(220 citation statements)

References 21 publications

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“…Previous studies assessing the acute effects of i.p. nicotine administration upon locomotion have yielded mixed results (either an increase or a decrease have been reported, see Jerome and Sanberg 1987;Clarke and Kumar 1983). Present data suggest an age-related dissociation in nicotine effects, which can possibly be ascribed to age-related discontinuities in the functional maturation of drug-targeted brain systems (Naeff et al 1992;Teicher et al 1995;Trauth et al 1999).…”

Section: Behavioral/pharmacological Effects Of Oral Nicotinementioning

confidence: 72%

Peculiar Vulnerability to Nicotine Oral Self-administration in Mice during Early Adolescence

Adriani

Macrı̀

Pacifici

et al. 2002

Neuropsychopharmacology

194

142

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(10 mg/l). After a 6-day period, a fading study was carried out, in which nicotine concentration was reduced to 7 mg/l (days 7-9) and 5 mg/l (days 10-12), to assess whether animals would compensate by increasing their intake from the nicotine solution. In Experiment 2, psychopharmacological effects on locomotion induced by the nicotine solution (0, 10, 30 mg/l) Recent research has emphasized that adolescence is associated with patterns of temporary deviance (Arnett 1992) and the use of various kinds of psychoactive agents (Mathias 1996). Drug abuse in adolescents ranging from 11-12 to 17-18 years of age is likely to start with tobacco smoking, which can be followed by marijuana and/or 1991;Breslau et al. 1993;Nides et al. 1995;Kandel and Chen 2000). Despite the social and scientific importance of deepening our knowledge of this issue (see e.g. Colby et al. 2000), there have been very few investigations on the psychobiological factors contributing to the specific adolescence-related willingness to experience various psychoactive drugs (for a review, see Laviola et al. 1999;Spear 2000). For the purpose of laboratory studies, a suitable animal model of human adolescence is available in rodents. Namely, periadolescence is classically defined as the ontogenetic period that encompasses the week preceding the onset of puberty and the first few days thereafter (Spear and Brake 1983). Periadolescent rodents differ markedly from adults in their spontaneous behavioral repertoire (Cirulli et al. 1996;Terranova et al. 1993;Meaney and Stewart 1981;Panksepp 1981). In fact, elevated levels of novelty seeking and a reduced behavioral and hormonal response to stress (Adriani et al. 1998;Adriani and Laviola 2000) are exhibited by animals around this age. A characteristic hyporesponsivity to the effects of an acute administration of psychostimulants (Spear and Brake 1983;Laviola et al. 1995;Bolanos et al. 1998;Adriani and Laviola 2000), a peculiar pattern of behavioral sensitization following repeated drug exposure (Laviola et al. 1995(Laviola et al. , 2001Adriani et al. 1998), as well as a weak drug-induced place conditioning profile (Adriani et al. 1998;Bolanos et al. 1996Bolanos et al. , 1998 but see Campbell and Spear 2000), are also reported. Based on these findings, an increased vulnerability to the addictive properties of abused drugs has been suggested to be typical of adolescence in both humans and animals models (see Laviola et al. 1999).In the present study, we were interested in nicotine, which beside being the main psychoactive compound implied in tobacco smoking, also shares most of the characteristics of other addictive drugs (Corrigall et al. 1992(Corrigall et al. ,1994Pontieri et al. 1996;Merlo-Pich et al. 1997;Stolerman 1999). Nicotine's effects in mice have been shown to be highly dependent on the genetic background (see Marks et al. 1989;Robinson et al. 1996). However, the interaction between the pharmacological effects and the incentive properties of nicotine during the adolescent period has been largel...

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Section: Behavioral/pharmacological Effects Of Oral Nicotinementioning

confidence: 72%

Peculiar Vulnerability to Nicotine Oral Self-administration in Mice during Early Adolescence

Adriani

Macrı̀

Pacifici

et al. 2002

Neuropsychopharmacology

194

142

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“…Previous research has shown that acute treatment with nicotine can suppress locomotor activity in rats [7,36,37]. Fig.…”

Section: Discussionmentioning

confidence: 87%

“…Importantly, although the shift measures differed statistically, overall activity for HR and LR (number of infrared beam breaks) after acute and chronic administration of nicotine did not differ significantly (Trial 1: HR = 179 ± 18, LR = 152 ± 10; Trial 7: HR = 382 ± 21, LR = 347 ± 12). This latter result is consistent with the z-score analyses; nicotine disrupts predictable individual differences in activity that are present in a drug-free state.We found that mecamylamine (1 mg/kg) completely prevented the acute suppressant and chronic activating effects of nicotine [7,26,37]. The peripheral nACh receptor antagonist hexamethonium, in contrast, did not block the chronic psychomotor effects of nicotine [5,7].…”

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confidence: 77%

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Individual differences in rat locomotor activity are diminished by nicotine through stimulation of central nicotinic acetylcholine receptors

Bevins¹,

Besheer²

2001

Physiology & Behavior

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Rats exposed to a small inescapable environment are more active when the environment is novel than when it is familiar (Refs. [23,33]; see later). Recently, the empirical and theoretical interest in the behavioral activating effect of novelty has increased. This interest is driven, in part, by evidence indicating that reactivity to a novel environment is a behavioral measure of a rat's sensitivity to stress. Rats exposed to a novel environment show an increase in plasma levels of the "stress hormone" corticosterone (e.g., Ref. [25]). Importantly, novelty-induced increases in corticosterone are greater in rats that display more locomotor activity to an inescapable novel environment [29]. Moreover, rats more activated by exposure to a novel environment [often termed high responders (FIR)] displayed a greater increase in corticosterone levels to restraint stress than rats that were less reactive to the novel environment [low responders (LR)]. HR also had a more prolonged increase in corticosterone to this restraint than LR [10]. This work is important because it demonstrates that a purported behavioral measure of stress sensitivity (i.e., novelty-induced activity) predicts the response to another form of stress (i.e., restraint).Reactivity to a novel environment has served as a predictive variable in recent drug abuse studies (see Refs. [9,31 ] for reviews). This predictive value is another reason for the recent interest in novelty-induced activity. For instance, rats that are more activated by exposure to a novel environment (HR) more readily self-administer amphetamine and are more sensitive to the locomotor-stimulant effects of amphetamine [29]. Novelty-induced activity has been found to also predict such behavioral effects as activity induced by cocaine and caffeine [16], ethanol-induced activity and ethanol self-administration [14,15], amphetamine-conditioned hyperactivity to contextual stimuli [17], cueing effects of amphetamine [13] and amphetamine barpress suppressant effects [6].Another factor contributing to the interest in novelty-induced activity is the potential insight it may provide into the behavioral and neural substrates underlying individual differences in drug abuse vulnerability. This idea is based, in part, on the assumption that the predictive relation just described likely refl ects an overlap in the mechanism(s) responsible Published in Physiology & Behavior 72 (2001) Abstract: An increasing body of research has focused on isolating factors that predict or alter individual differences in the behavioral and neural processes mediating the effects of abused drugs. Within this framework, the current report assessed individual differences and the locomotor effect of nicotine. Rats were screened for activity induced by a novel environment. Rats, which were more active to initial environment exposure, remained more active even after seven additional 30-min exposures to the same environment. Treatment with nicotine-di-D tartrate (1 mg/kg, sc) disrupted this effect. This nicotine disruption of indiv...

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“…Similarly, nicotine administration also modifies locomotion, anxiety, memory, nociception, and produces rewarding effects in several animal models (Clarke and Kumar, 1983;Hildebrand et al, 1999;Marubio et al, 1999;Picciotto et al, 1995). Neuroanatomical studies have shown a high density of CB1 receptors in neurons of the cerebellum, basal ganglia, limbic cortices, hippocampus, 3 hypothalamus and different nuclei of the extended amygdala (Tsou et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

Role of the cannabinoid system in the effects induced by nicotine on anxiety-like behaviour in mice

2006

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Rationale: Acute behavioural effects and motivational responses induced by nicotine can be modulated by the endocannabinoid system supporting the existence of a physiological interaction between these two systems. Objectives: The present study was designed to examine the possible involvement of the cannabinoid system in the anxiolytic-and anxiogenic-like responses induced by nicotine in mice. Methods:

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

Cited by 424 publications

References 21 publications

Peculiar Vulnerability to Nicotine Oral Self-administration in Mice during Early Adolescence

Peculiar Vulnerability to Nicotine Oral Self-administration in Mice during Early Adolescence

Individual differences in rat locomotor activity are diminished by nicotine through stimulation of central nicotinic acetylcholine receptors

Role of the cannabinoid system in the effects induced by nicotine on anxiety-like behaviour in mice

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