Effects of smoking on acoustic startle and prepulse inhibition in humans

Duncan, Erica; Madonick, Steven; Chakravorty, Subhajit; Parwani, Arti; Szilágyi, Sándor; Efferen, Toby R.; Gonzenbach, Stephen; Angrist, Burt; Rotrosen, John

doi:10.1007/s002130100719

Cited by 88 publications

(77 citation statements)

References 20 publications

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“…The nicotine effect on PPI was primarily on the startlealone response (Figure 1, middle panel), which was consistent with several previous reports in humans and rodents (Acri et al, 1995;Faraday et al, 1999;Duncan et al, 2001). We did not find significant nicotinic effect in reducing response amplitude in prepulse-pulse trials.…”

Section: Discussionsupporting

confidence: 92%

“…This suggests that the nicotine-induced transient enhancement on PPI in schizophrenia patients was not likely due to medications that patients were taking. Previous studies have also demonstrated that nicotine enhances PPI in nonsmoker controls, which supports the conclusion that the nicotinic effect on PPI is not simply to reverse the effect of nicotine withdrawal, but rather it has an impact on the mechanism of PPI (Kumari et al, 1997;Duncan et al, 2001;Postma et al, 2006).…”

Section: Discussionsupporting

confidence: 75%

“…However, other studies have shown no effect, or even the opposite effect (Decker et al, 1997;Faraday et al, 1999;Mirza et al, 2000;Schreiber et al, 2002). Several studies in healthy humans have generally affirmed the nicotinic enhancement of PPI (Kumari et al, 1996;Della Casa et al, 1998;Duncan et al, 2001), but the opposite effect has also been reported in studies using cigarettes with high nicotine content (Hutchison et al, 2000).…”

Section: Introductionmentioning

confidence: 98%

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Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients

Hong

Wonodi

Lewis

et al. 2007

Neuropsychopharmacol

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Acoustic prepulse inhibition (PPI) is considered an important biomarker in animal studies of psychosis and a number of psychiatric conditions. Nicotine has been shown to improve acoustic PPI in some animal strains and in humans. However, there is little data on effects of nicotine on acoustic PPI in schizophrenia patients using a double-blind, placebo-controlled study design. The primary aim of the current study was to test the effect of nicotine nasal spray on acoustic PPI in schizophrenia patients. The secondary aim was to test nicotine effect on prepulse facilitation (PPF). The study included 18 schizophrenia patient smokers and 12 healthy control smokers, tested in a double-blind, placebo-controlled, crossover, randomized design immediately after nicotine or saline placebo nasal sprays. PPI was tested using 120 ms prepulse-pulse interval. PPF was tested using 4500 ms prepulse-pulse interval. The results showed a significant main effect of drug on PPI in that nicotine improved PPI compared to placebo (p ¼ 0.008) with no drug by diagnosis interaction (p ¼ 0.90). Improvement in PPI in response to nicotine was significantly correlated with the baseline severity of clinical symptoms (r ¼ 0.59, p ¼ 0.02) in patients. There was no significant drug or drug by diagnosis interaction for the 4500 ms prepulse-pulse interval condition. However, nicotine improved inhibition in a subgroup of subjects exhibiting PPF (p ¼ 0.002). In conclusion, the findings confirmed that nicotine transiently improves acoustic PPI in schizophrenia patients. Additionally, schizophrenia patients with more clinical symptoms may have benefited more from nicotinic effect on PPI.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 98%

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Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients

Hong

Wonodi

Lewis

et al. 2007

Neuropsychopharmacol

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“…PPI is a phenomenon in which a low threshold initial stimulus, called a pre-pulse, suppresses subsequent responding to a startling stimulus [40] and is used as a measure of sensory gating [2,23,79]. Acute nicotine enhances PPI in smokers and non-smokers in humans [17][18][19] and animals [2,30]. In humans, withdrawal from chronic nicotine is associated with deficits in PPI that can be reversed by an acute dose of nicotine [45].…”

Section: Introductionmentioning

confidence: 99%

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

André

Gulick

Portugal

et al. 2008

Behavioural Brain Research

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Nicotine withdrawal is associated with multiple symptoms such as anxiety, increased appetite, and disrupted cognition in humans. Although animal models have provided insights into the somatic and affective symptoms of nicotine withdrawal, less research has focused on the effects of nicotine withdrawal on cognition. Therefore, in this study, C57BL/6 mice were used to test the effects of withdrawal from chronic nicotine on foreground and background contextual fear conditioning, which present the context as a primary or secondary stimulus, respectively. Mice withdrawn from 12 days of chronic nicotine (6.3 mg/kg/day) or saline were trained and tested in either foreground or background contextual fear conditioning; nicotine withdrawal-associated deficits in contextual fear conditioning were observed in both conditions. Mice were also tested for the effects of withdrawal on pre-pulse inhibition of the acoustic startle reflex (PPI), a measure of sensory gating, and on the acoustic startle reflex. Mice withdrawn from 12 days of chronic nicotine (6.3 or 12.6 mg/kg/day) or saline underwent one 30-minute PPI and startle session; no effect of withdrawal from chronic nicotine on PPI or startle was observed for either dose at 24 hours after nicotine removal. Therefore, mice were tested at different time points following withdrawal from 12.6 mg/kg/day chronic nicotine (8, 24, and 48 hours after nicotine removal). No effect of withdrawal from chronic nicotine was observed at any time point for PPI. Overall, these results demonstrate that nicotine withdrawal disrupts two methods of contextual learning but not sensory gating in C57BL/6 mice.

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“…Nicotine, an agonist of nicotinic acetylcholine receptors (nAChR), consistently enhances PPI in humans (Baschnagel and Hawk 2008;Della Casa et al 1998;Duncan et al 2001; Kumari et al 1996;Kumari et al 1997) and animals (Acri et al 1995;Acri et al 1994;Curzon et al 1994;Faraday et al 1999;Schreiber et al 2002;Spielewoy and Markou 2004) The exact mechanism by which nicotine enhances PPI is not yet understood but one way nicotine may improve PPI is by enhancing the diminishment of the processing of the pulse suggesting that nicotine may improve stimulus filtering (Baschnagl and Hawk 2008). In mice, the PPI-enhancing effect of nicotine is strain dependent (Faraday et al 1999) suggesting genetic influences in nicotine-induced modulation of PPI (Kumari and Postma 2005).…”

Section: Introductionmentioning

confidence: 99%

The effect of nicotine on sensorimotor gating is modulated by a CHRNA3 polymorphism

et al. 2013

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RATIONALE: Prepulse inhibition (PPI) of the acoustic startle response, a measure of sensorimotor gating, can be enhanced by nicotine. Moreover, the TT genotype of the nicotinic acetylcholine receptor (nAChR) 3-subunit (CHRNA3) rs1051730 polymorphism has previously been associated with diminished PPI and nicotine dependence. OBJECTIVES: We tested whether this CHRNA3 polymorphism also modulates the nicotine-induced enhancement of PPI. METHODS: We assessed the effect of nicotine on PPI, startle reactivity, and habituation in 52 healthy nonsmoking volunteers genotyped for CHRNA3 rs1051730 in a double-blind, placebo-controlled, counterbalanced, within-subjects design. Additionally, cotinine plasma levels were measured. RESULTS: Nicotine significantly enhanced PPI in TT homozygotes only and tended to worsen PPI in TC and CC carriers. Additionally, nicotine significantly reduced startle habituation. CONCLUSIONS: The present findings imply that the effect of nicotine on sensorimotor gating is modulated by nAChR 3-subunits. Thus, genetic variation in nicotinic receptor genes might be an important connecting link between early attentional processes and smoking behavior.

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Effects of smoking on acoustic startle and prepulse inhibition in humans

Abstract: Smoking after overnight washout from cigarettes enhanced sensorimotor gating compared to pre-smoking values and compared to gating in non-smokers.

Cited by 88 publications

References 20 publications

Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients

Nicotine Effect on Prepulse Inhibition and Prepulse Facilitation in Schizophrenia Patients

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

The effect of nicotine on sensorimotor gating is modulated by a CHRNA3 polymorphism

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