Nicotine-induced impulsive action

Kirshenbaum, Ari P.; Jackson, Eric R.; Brown, Seth J.; Fuchs, Jason R.; Miltner, Betsie C.; Doughty, Adam H.

doi:10.1097/fbp.0b013e328345ca1c

Cited by 24 publications

(14 citation statements)

References 46 publications

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“…This result suggests that acute nicotine reduces response inhibition capacity in both strains. Although this finding is inconsistent with our expectations, it is consistent with nicotine-induced reductions in IRTs observed in DRL studies using Sprague Dawley rats (Kirshenbaum et al 2008, 2009, 2011). Performance in DRL schedules cannot be readily interpreted in terms of response inhibition capacity, because it is also sensitive to reinforcer-efficacy manipulations (e.g., reinforcer magnitude; Doughty and Richards 2002).…”

Section: Discussioncontrasting

confidence: 83%

“…Unlike humans, acute nicotine administration in rodents consistently decreases response inhibition capacity in a wide range of tasks, including the 5-CSRTT (Bizarro et al 2004; Blondel et al 2000; Hahn et al 2002; Semenova et al 2007), the differential reinforcement of low rates (DRL) schedule of reinforcement (Kirshenbaum et al 2011; Kirshenbaum et al 2009; Kirshenbaum et al 2008; Popke et al 2000a; Popke et al 2000b), the stop-signal task (Kirshenbaum et al 2011), and the go/no-go discrimination (Kolokotroni et al 2011). Only the temporal response differentiation task, which involves holding down a lever for a target interval, appears to be insensitive to nicotine-induced premature responding (Popke et al 2000b).…”

Section: Introductionmentioning

confidence: 99%

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Detrimental effects of acute nicotine on the response-withholding performance of spontaneously hypertensive and Wistar Kyoto rats

et al. 2014

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Rationale Attention-Deficit Hyperactivity Disorder (ADHD) is associated with a higher prevalence of smoking, which may be related to potential therapeutic effects of nicotine on ADHD symptoms. Whereas nicotine offers robust improvements in sustained attention, the effects of nicotine on impulsivity are unclear. Objectives The present study examined the effects of nicotine on the response inhibition capacity of spontaneously hypertensive rats (SHR), an animal model of ADHD, compared to that of a normotensive control Wistar Kyoto (WKY) using the Fixed Minimum Interval (FMI) schedule of reinforcement. Methods Tests were conducted following acute injections of subcutaneous nicotine (0.1 – 0.6 mg/kg). On each FMI trial, the first lever press initiated an inter-response time (IRT); a head entry into a food receptacle terminated the IRT. IRTs longer than 6 s were intermittently reinforced with sucrose. Results A model that assumes that only a proportion of IRTs are sensitive to the timing contingencies of the FMI provided a close fit to the data, regardless of strain or treatment. No baseline difference in FMI performance was observed between SHR and WKY. Nicotine reduced the duration of timed IRTs and the duration of latencies to the IRT-initiating lever press similarly for both strains. Nicotine dose-dependently increased the proportion of timed IRTs; the dose-response curve was shifted leftwards in SHR relative to WKY. Conclusions These results suggest that nicotine (a) reduces response-inhibition capacity (b) enhances the reinforcement efficacy of sucrose, and (c) dose-dependently enhances attention-like sensitivity to contingencies of reinforcement, through mechanisms that are yet unknown.

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Section: Discussioncontrasting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Detrimental effects of acute nicotine on the response-withholding performance of spontaneously hypertensive and Wistar Kyoto rats

et al. 2014

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“…The observed effect of nicotine on the response-threshold is also consistent with the effects of nicotine on the performance of rats in other timing tasks that involve response withholding, such as the lever-holding task (Popke, Mayorga, Fogle, & Paule, 2000), the fixed-minimum interval schedule of reinforcement (Mazur et al, 2014), and the differential reinforcement of low rates schedule (Kirshenbaum, Jackson, Brown, Fuchs, Miltner, Doughty, 2011; Kirshenbaum, Johnson, Schwarz, & Jackson, 2009; Kirshenbaum, Brown, Hughes, Doughty, 2008; Popke et al, 2000). In these tasks, animals must withhold a response for a fixed interval to obtain reinforcement, and typically produce withholding intervals that are close to the withholding requirement.…”

Section: Discussionsupporting

confidence: 76%

Revisiting the effect of nicotine on interval timing

Daniels

Watterson

Garcia

et al. 2015

Behavioural Brain Research

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This paper reviews the evidence for nicotine-induced acceleration of the internal clock when timing in the seconds-to-minutes timescale, and proposes an alternative explanation to this evidence: that nicotine reduces the threshold for responses that result in more reinforcement. These two hypotheses were tested in male Wistar rats using a novel timing task. In this task, rats were trained to seek food at one location after 8 s since trial onset and at a different location after 16 s. Some rats received the same reward at both times (group SAME); some received a larger reward at 16 s (group DIFF). Steady baseline performance was followed by 3 days of subcutaneous nicotine administration (0.3 mg/kg), baseline recovery, and an antagonist challenge (mecamylamine, 1.0 mg/kg). Nicotine induced a larger, immediate reduction in latencies to switch (LTS) in group DIFF than in group SAME. This effect was sustained throughout nicotine administration. Mecamylamine administration and discontinuation of nicotine rapidly recovered baseline performance. These results support a response-threshold account of nicotinic disruption of timing performance, possibly mediated by nicotinic acetylcholine receptors. A detailed analysis of the distribution of LTSs suggests that anomalous effects of nicotine on LTS dispersion may be due to loss of temporal control of behavior.

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“…Nicotine has been shown to produce disinhibitory behavior in the rats after subchronic peripheral nicotinic acetylchline receptor blockage (Ericson et al, 2000). It has also been suggested that response disinhibition in the variable-interval differential reinforcement of low rate responding and stop signal tasks are related in a systematic manner to nicotinic-acetylcholine receptor activation (Kirshenbaum et al, 2011). Thus it is possible that the loss of cholinergic tone produced by adolescent alcohol exposure seen in the present study could result in a “sensitization” of nicotinic receptors that promote the expression of disinhibitory behaviors under the conditions of stress/ food restriction such as those that occur in the modified open field conflict test.…”

Section: 0 Discussionmentioning

confidence: 99%

Periadolescent ethanol exposure reduces adult forebrain ChAT+IR neurons: correlation with behavioral pathology

et al. 2011

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Substance abuse typically begins in adolescence; therefore, the impact of alcohol during this critical time in brain development is of particular importance. Epidemiological data indicate that excessive alcohol consumption is prevalent among adolescents and may have lasting neurobehavioral consequences. Loss of cholinergic input to the forebrain has been demonstrated following fetal alcohol exposure and in adults with Wernicke-Korsakoff syndrome. In the present study, immunohistochemistry for choline acetyltransferase (ChAT) was determined to assess forebrain cholinergic neurons (Ch1–4), and behavioral changes following periadolescent alcohol exposure. Wistar rats were exposed to intermittent ethanol vapor (14 hrs on/10 hrs off/day) for 35 days from PD 22-PD 57 (average blood alcohol concentration (BAC): 163 mg%). Rats were withdrawn from vapor and assessed for locomotor activity, startle response, conflict behavior in the open field, and immobility in the forced swim test, as adults. Rats were then sacrificed at day 71/72 and perfused for histochemical analyses. Ethanol vapor exposed rats displayed: increased locomotor activity 8 hrs after the termination of vapor delivery for that 24 hr period at day 10 and day 20 of alcohol vapor exposure, significant reductions in the amplitude of their responses to prepulse stimuli during the startle paradigm at 24 hrs withdrawal, and at two weeks following withdrawal, less anxiety-like and/or more “disinhibitory” behavior in the open field conflict, and more immobility in the forced swim test. Quantitative analyses of ChAT immunoreactivity revealed a significant reduction in cell counts in the Ch1–2 and Ch3–4 regions of the basal forebrain in ethanol vapor exposed rats. This reduction in cell counts was significantly correlated with less anxiety-like and/or more “disinhibitory” behavior in the open field conflict test. These studies demonstrate that behavioral measures of arousal, affective state, disinhibitory behavior and ChAT+IR, are all significantly impacted by periadolescent ethanol exposure and withdrawal in Wistar rats.

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Nicotine-induced impulsive action

Cited by 24 publications

References 46 publications

Detrimental effects of acute nicotine on the response-withholding performance of spontaneously hypertensive and Wistar Kyoto rats

Detrimental effects of acute nicotine on the response-withholding performance of spontaneously hypertensive and Wistar Kyoto rats

Revisiting the effect of nicotine on interval timing

Periadolescent ethanol exposure reduces adult forebrain ChAT+IR neurons: correlation with behavioral pathology

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