Effects of smoking on the acoustic startle response and prepulse inhibition in smokers with and without posttraumatic stress disorder

Vrana, Scott R.; Calhoun, Patrick S.; McClernon, F. Joseph; Dennis, Michelle F.; Lee, Sherman T.; Beckham, Jean C.

doi:10.1007/s00213-013-3181-y

Cited by 26 publications

(30 citation statements)

References 53 publications

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“…Other studies of ASR latency and magnitude in PTSD have not reached a consensus. While the association between PTSD and longer startle latency in our population contrasts with a study conducted by Vrana et al, which found faster latency in PTSD, that study did not consider the effects of TOXO (Vrana et al 2013). The literature on ASR magnitude in PTSD is also inconclusive.…”

Section: Discussioncontrasting

confidence: 99%

Relationship between Toxoplasma gondii seropositivity and acoustic startle response in an inner-city population

Massa

Duncan

Jovanović

et al. 2017

Brain, Behavior, and Immunity

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Toxoplasma gondii (TOXO) is a neuroinvasive protozoan parasite that induces the formation of persistent cysts in mammalian brains. It infects approximately 1.1 million people in the United States annually. Latent TOXO infection is implicated in the etiology of psychiatric disorders, especially schizophrenia (Scz), and has been correlated with modestly impaired cognition. The acoustic startle response (ASR) is a reflex seen in all mammals. It is mediated by a simple subcortical circuit, and provides an indicator of neural function. We previously reported the association of TOXO with slowed acoustic startle latency, an index of neural processing speed, in a sample of schizophrenia and healthy control subjects. The alterations in neurobiology with TOXO latent infection may not be specific to schizophrenia. Therefore we examined TOXO in relation to acoustic startle in an urban, predominately African American, population with mixed psychiatric diagnoses, and healthy controls. Physiological and diagnostic data along with blood samples were collected from 364 outpatients treated at an inner-city hospital. TOXO status was determined with an ELISA assay for TOXO-specific IgG. A discrete titer was calculated based on standard cut-points as an indicator of seropositivity, and the TOXO-specific IgG concentration served as serointensity. A series of linear regression models were used to assess the association of TOXO seropositivity and serointensity with ASR magnitude and latency in models adjusting for demographics and psychiatric diagnoses (PTSD, major depression, schizophrenia, psychosis, substance abuse). ASR magnitude was 11.5% higher in TOXO seropositive subjects compared to seronegative individuals (p=0.01). This effect was more pronounced in models with TOXO serointensity that adjusted for sociodemographic covariates (F=7.41, p=.0068; F=10.05, p=0.0017), and remained significant when psychiatric diagnoses were stepped into the models. TOXO showed no association with startle latency (t=0.49, p=0.63) in an unadjusted model, nor was TOXO associated with latency in models that included demographic factors. After stepping in individual psychiatric disorders, we found a significant association of latency with a diagnosis of PTSD (F=5.15, p=0.024), but no other psychiatric diagnoses, such that subjects with PTSD had longer startle latency. The mechanism by which TOXO infection is associated with high startle magnitude is not known, but possible mechanisms include TOXO cyst burden in the brain, parasite recrudescence, or molecular mimicry of a host epitope by TOXO. Future studies will focus on the neurobiology underlying the effects of latent TOXO infection as a potential inroad to the development of novel treatment targets for psychiatric disease.

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Section: Discussioncontrasting

confidence: 99%

Relationship between Toxoplasma gondii seropositivity and acoustic startle response in an inner-city population

Massa

Duncan

Jovanović

et al. 2017

Brain, Behavior, and Immunity

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“…Further, research shows that persons with PTSD show especially heightened anxiety in response to stressors and smoking appears to reduce such distress (Beckham et al, 2005, 2007). We believe that smoking may reduce heightened anxiety amongst persons with PTSD either directly (Hogle et al, 2010), or via its effects on attentional processing or by mitigating sensorimotor gating deficits (Baschnagel & Hawk, 2008; Calhoun et al, 2011; Vrana et al, 2013). Some research fails to show that smoking reduces acoustically elicited startle in smokers with PTSD, casting doubt on the notion that smoking exerts anxiolytic effects.…”

Section: Discussionmentioning

confidence: 99%

“…Some research fails to show that smoking reduces acoustically elicited startle in smokers with PTSD, casting doubt on the notion that smoking exerts anxiolytic effects. However, those results may be challenged on the bases of the timing of the smoking experience in those studies and the fact that the startle paradigm may have primarily activated fear and not anxiety (Calhoun et al, 2011; Vrana et al, 2013), with the latter likely being more sensitive to smoking effects (Hogle et al, 2010; Jonkman et al, 2008). In short, we believe that smokers with PTSD are likely to show especially strong anxiety reactions to stressful stimuli, and that nicotine can quell such reactions (Beckman et al, 2005, 2007).…”

Section: Discussionmentioning

confidence: 99%

Smoking-induced affect modulation in nonwithdrawn smokers with posttraumatic stress disorder, depression, and in those with no psychiatric disorder.

Cook¹,

Baker²,

Beckham³

et al. 2017

Journal of Abnormal Psychology

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This research sought to determine whether smoking influences affect by means other than withdrawal reduction. Little previous evidence suggests such an effect. We surmised that such an effect would be especially apparent in posttraumatic stress disorder (PTSD) and major depressive disorder (MDD), two disorders that are frequently comorbid with smoking and that involve dysregulated affect. Participants were US veterans who were regular smokers (N=159): 52 with PTSD (58% with comorbid MDD); 51 with MDD, and 56 controls with no psychiatric disorder. During three positive and three negative mood induction trials (scheduled over two sessions), non-withdrawn participants smoked either a nicotine-containing cigarette (NIC+), a nicotine-free cigarette (NIC−), or held a pen. Positive and negative affect were each measured before and after mood induction. Results showed a significant 2-way interaction of smoking condition x time on negative affect during the negative mood induction [F(6, 576)=2.41, p=.03] in those with PTSD and controls. In these groups, both NIC+ and NIC−, relative to pen, produced lower negative affect ratings following the negative mood induction. There was also a 2-way interaction of smoking condition x time on positive affect response to the positive mood induction amongst those with PTSD and controls F(6, 564)=3.17, p= .005] and amongst MDD and controls [F(6, 564)=2.27, p= .036]. Amongst all smokers, NIC+ enhanced the magnitude and duration of positive affect more than did NIC−. Results revealed affect modulation outside the context of withdrawal relief; such effects may motivate smoking among those with psychiatric diagnoses, and among smokers in general.

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“…Evidence suggests that one symptom cluster in PTSD, emotional numbing, a negative symptom similar to depression, is strongly associated with smoking frequency and difficulty quitting (Greenberg et al, 2012). Similarly, acoustic startle, which may reflect baseline arousal, isx enhanced in PTSD patients and by nicotine, but smoking cessation results in decreased startle (Vrana et al, 2013). Hyper arousal, another symptom cluster in PTSD, is shown to be reduced by nicotine (Beckham et al, 2007).…”

Section: Post-traumatic Stress Disorder and Drug Abusementioning

confidence: 99%

Substance abuse, memory, and post-traumatic stress disorder

Tipps

Raybuck

Lattal

2014

Neurobiology of Learning and Memory

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A large body of literature demonstrates the effects of abused substances on memory. These effects differ depending on the drug, the pattern of delivery (acute or chronic), and the drug state at the time of learning or assessment. Substance use disorders involving these drugs are often comorbid with anxiety disorders, such as post-traumatic stress disorder (PTSD). When the cognitive effects of these drugs are considered in the context of the treatment of these disorders, it becomes clear that these drugs may play a deleterious role in the development, maintenance, and treatment of PTSD. In this review, we examine the literature evaluating the cognitive effects of three commonly abused drugs: nicotine, cocaine, and alcohol. These three drugs operate through both common and distinct neurobiological mechanisms and alter learning and memory in multiple ways. We consider how the cognitive and affective effects of these drugs interact with the acquisition, consolidation, and extinction of learned fear, and we discuss the potential impediments that substance abuse creates for the treatment of PTSD.

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Effects of smoking on the acoustic startle response and prepulse inhibition in smokers with and without posttraumatic stress disorder

Cited by 26 publications

References 53 publications

Relationship between Toxoplasma gondii seropositivity and acoustic startle response in an inner-city population

Relationship between Toxoplasma gondii seropositivity and acoustic startle response in an inner-city population

Smoking-induced affect modulation in nonwithdrawn smokers with posttraumatic stress disorder, depression, and in those with no psychiatric disorder.

Substance abuse, memory, and post-traumatic stress disorder

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