Nicotine usage is associated with elevated processing speed, spatial working memory, and visual learning performance in youth at ultrahigh-risk for psychosis

Gupta, Tina; Mittal, Vijay A.

doi:10.1016/j.psychres.2014.07.085

Cited by 10 publications

(12 citation statements)

References 36 publications

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“…Nicotine and nicotinic agonists have been shown to significantly improve attention (Allison and Shoaib 2012), fear memory (Tian et al 2010;Lima et al 2013), and working memory (Levin and Simon 1998). Although nicotinic systems have been shown in numerous studies to be important for spatial working memory (SWM) in animals (Levin et al 2005;Fisher et al 2011;Mizoguchi et al 2011) and humans (Smith et al 2002;Sacco et al 2005;Wing et al 2011;Gupta and Mittal 2014), the brain regions and the mechanisms involved in nicotine-induced SWM alteration are less well known.…”

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confidence: 99%

Activation of matrix metalloproteinase in dorsal hippocampus drives improvement in spatial working memory after intra‐VTA nicotine infusion in rats

Shu

鄭

Wang

et al. 2015

Journal of Neurochemistry

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The hippocampus receives dopaminergic projections from the ventral tegmental area (VTA) and substantia nigra. These inputs appear to provide a modulatory signal that influences hippocampus-dependent behaviors. Enhancements in working memory performance have been previously reported following acute smoking/nicotine exposure. However, the underlying mechanism remains unclear. This study investigated the effects of nicotine on spatial working memory (SWM) and the mechanisms involved. Delayed alternation T-maze task was used to assess SWM. In situ and gel gelatin zymography were used to detect matrix metalloproteinase-9 (MMP-9) in SWM. Systemic or local (intra-VTA) administration of nicotine significantly improves SWM, which was accompanied by increased MMP-9 activity in dorsal hippocampus (dHPC). Intra-dHPC administration of MMP inhibitor FN-439 abolished the memory enhancement induced by intra-VTA nicotine infusion. FN-439 had no effect on locomotor behavior. Our data suggest that intra-VTA nicotine infusion activates MMP-9 in dHPC to improve SWM in rats.

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confidence: 99%

Activation of matrix metalloproteinase in dorsal hippocampus drives improvement in spatial working memory after intra‐VTA nicotine infusion in rats

Shu

鄭

Wang

et al. 2015

Journal of Neurochemistry

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“…In the study conducted by Cadenhead, prevalence of current smokers was found to be 18% in at-risk individuals (N=89) and 32% in early psychosis patients (N=75) (converted to psychosis-and therefore no longer prodromal within the past 2 years) versus 14.1% in the control nonpsychiatric group (N=85) 53. Another estimate is provided by Gupta and Mittal,54 in a smaller sample, where UHR patients (N=35) reported nicotine use at a rate of 46% versus the 22% of the control group (N=32, P ≤0.05) 54. In the study of Buchy et al, the rate of tobacco use in a sample of Clinical High Risk (CHR) individuals (N=170) was 33.3%, with 2.8% corresponding to dependence or abuse 55.…”

Section: Resultsmentioning

confidence: 96%

“…Risk did not decline as the time to schizophrenia onset increased, suggesting that the association is not substantially attributed to the presence of a prodrome.Cadenhead (2011)53Case control, longitudinal studyThe Cognitive Assessment and Risk Evaluation (CARE) program, University of California San Diego249 [75 Early Psychosis (76.0% males), 89 At Risk for psychosis patients (60.7% males) and 85 nonpsychiatric control subjects (45.9% males)]DSM-IV or the Schedule for Affective Disorders and Schizophrenia for School-Age ChildrenStructured Interview for Prodromal Symptoms (SIPS)Development of psychosis per the SCID/KSADS criteriaClinical Interview. Dichotomous variable for current tobacco use: Yes/NoANOVA was repeated with tobacco and cannabis use as between subjects factors; subjects with current substance misuse excludedReduced Prepulse Inhibition (PPI) in early psychosis patients who smoke compared to nonsmokers; increased PPI in at risk subjects who smoke compared to nonsmokersGupta and Mittal (2014)54Cross-sectional, case control studyAdolescent Development and Preventive Treatment (ADAPT) program67 [35 Ultra High Risk (UHR) (63% males) and 32 Healthy Control, (HC) subjects (41% males)DSM-IVAttenuated Positive Symptom (APS) or Genetic Risk and Deterioration (GRD) prodromal syndromesNot applicableAlcohol/Drug Use Scale (AUS/DUS)Substance dependence disorder was exclusion criterionUHR subjects smoked more frequently than HC subjects, 46% vs 22%; Elevated cognitive performance in UHR smokers vs UHR nonsmokersZhang et al (2012)51Cross-sectional case control studyInpatients in the Beijing Hui-Long-Guan Psychiatric Hospital1336 (776 male patients with schizophrenia, 560 male healthy controls)DSM-IVNot specifiedNot specified- presumably conferred by the recorded illness course durationPatient,Questionnaire,Fagerstrom Test for Nicotine Dependence (FTND)Participants reported no dependence on any substance other than tobaccoMean age of smoking initiation 7 years (SD=10.2) before psychosis onset, during the early prodromal or premorbid period. Positive correlation between age at starting smoking and age at onset of illness ( P =0.005)Buchy et al (2014)55Longitudinal study/cross-sectional as for the substance use measuresMulti-site NIMH study “Enhancing the Prospective Prediction of Psychosis”(PREDICT),170 (96 men, 74 women) at Clinical High Risk (CHR) of psychosisNot applicable…”

Section: Resultsmentioning

confidence: 99%

<p>Nicotine consumption during the prodromal phase of schizophrenia – a review of the literature</p>

Γώγος

Σκώκου

Ferentinou

et al. 2019

NDT

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Recent research has fueled a debate concerning the role of nicotine in the emergence of schizophrenia. The three main hypotheses are: (a) the self-medication effect, (b) the causal relationship hypothesis, or (c) the shared diathesis hypothesis. To explore this role, the study of nicotine consumption during the initial prodromal phase of schizophrenia offers important opportunities. In the present work, 10 relevant studies are reviewed, out of 727 retrieved citations, in order to address questions regarding the prevalence of smoking in the prodromal period, the time of smoking initiation, existing patterns of tobacco use in relation with the escalation of prodromal symptoms into first psychotic episode, and potential differences in symptomatology between smokers and nonsmokers. Even though there was considerable heterogeneity among studies, relevant findings are discussed. Prevalence of nicotine use during the prodromal period was reported to be 16.6–46%. Tobacco use was found to be taken up most often before or during the prodromal period of schizophrenia. Even though a protective role of smoking has been reported by one study, other studies report an increased risk for psychosis, with hazard ratios 2.77 (95% CI: 2.34–3.43) and 2.21 (95% CI: 1.11–4.42) for female and male heavy smokers (11–20 and >20 cigarettes/day), respectively. In a different study, the risk of onset was associated with the progressive use of cannabis and tobacco prior to onset, particularly with rapid escalation to the highest levels of use. Also, nicotine use in ultra high risk (UHR) for developing psychosis subjects is associated with elevated cognitive performance, namely better processing speed, visual learning, and spatial working memory. As a conclusion, it appears that evidence accumulates supporting a possible etiologic role of smoking, in the emergence of schizophrenia along with diverse effects on patients’ symptomatology, already demonstrable at the prodromal phase. Future research employing better-defined criteria should further explore the patterns of use and effects of nicotine during the schizophrenia prodrome.

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“…They recorded significant improvements in information processing [22]. Several studies have shown that nicotine use may help to improve cognitive deficits in the population of schizophrenia patients [23,24], especially because as much as 72-90% of this population smoke cigarettes [25].…”

Section: Discussionmentioning

confidence: 99%

Prolonged exposure to transdermal nicotine improves memory in male mice, but impairs biochemical parameters in male and female mice

Nieradko-Iwanicka

Pietraszek

Pośnik

et al. 2019

Ann Agric Environ Med.

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Introduction. Nicotine is an alkaloid that affects the functioning of the central nervous system and produces dependence. In low doses, it acts as a stimulant and relaxant. Nicotine was reported to have pro-cognitive effects in humans and animals. However, high doses of nicotine are harmful for many organs.The aim of the study was to check whether a 30-day exposure to transdermal nicotine affects memory and biochemical parameters in mice. Materials and method. A total of 32 mice (16 males and 16 females) were used in the experiment. Mice were divided into 4 groups of 8 animals each: I control-females receiving placebo patches for 30 days, II females receiving nicotine patches for 30 days, III control-males receiving placebo patches, IV males receiving nicotine patches. Spontaneous alternation and locomotor activity were examined weekly in a Y-maze. Body mass was recorded daily. On day 30, venous blood samples were obtained and the animals were anaesthetized with CO 2. Their blood was used to measure alanine transaminase (ALT), asparagine transaminase (AST), cholesterol, creatinine and glycosylated haemoglobin (HbA 1 C). Results. Nicotine significantly improved memory in male mice on day 8. It increased ALT and AST activities in males and females, as well as the concentration of cholesterol in their blood sera. Conclusions. In conclusion, transdermal nicotine may produce transient improvement in fresh spatial memory in male mice, but it is not a long-term effect and therefore nicotine does not seem to be appropriate for use in the treatment of neurodegenerative disorders. It elevates blood cholesterol level and thus may increase the risk of atherosclerosis and cardiovascular events; moreover, it negatively affects liver enzymes. Nicotine use is therefore not recommended.

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Nicotine usage is associated with elevated processing speed, spatial working memory, and visual learning performance in youth at ultrahigh-risk for psychosis

Cited by 10 publications

References 36 publications

Activation of matrix metalloproteinase in dorsal hippocampus drives improvement in spatial working memory after intra‐VTA nicotine infusion in rats

Activation of matrix metalloproteinase in dorsal hippocampus drives improvement in spatial working memory after intra‐VTA nicotine infusion in rats

<p>Nicotine consumption during the prodromal phase of schizophrenia – a review of the literature</p>

Prolonged exposure to transdermal nicotine improves memory in male mice, but impairs biochemical parameters in male and female mice

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