Mecamylamine blocks nicotine-induced enhancement of the P20 auditory event–related potential and evoked gamma

Phillips, Jennifer M.; Ehrlichman, Richard S.; Siegel, Steven J.

doi:10.1016/j.neuroscience.2006.11.003

Cited by 49 publications

(53 citation statements)

References 59 publications

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“…One might ask whether the reduced gamma synchrony at rest and other abnormalities in gamblers could be attributed to smoking as a confounding variable. This is highly unlikely a priori, because nicotine addiction has been demonstrated to be linked to increased gamma synchronization (39), rather than decreased as we see here, and because power spectra are generally unaffected by smoking habits (40,41). In a separate study on an extended nongambling control group, we compared power at the ACC, PCC, and right V1 sites and gamma synchronization between the ACC and PCC and found no difference between smokers and nonsmokers.…”

Section: Discussionmentioning

confidence: 59%

Altered paralimbic interaction in behavioral addiction

Thomsen

Joensson

Lou

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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The introduction of magnetoencephalography has made it possible to study electromagnetic signaling in deeper, paralimbic cortical structures such as the medial prefrontal/anterior cingulate (ACC) and medial parietal/posterior cingulate (PCC) cortices. Self-awareness and self-control have been attributed to these regions. To test the hypothesis that they are dysfunctional in pathological gambling with poor self-control, we studied gamblers with and without previous stimulant abuse and age-and sex-matched controls. We found that pathological gamblers were more impulsive than controls in a stopsignal task and attributed this to changes in the activity of the paralimbic network: Pathological gamblers had reduced synchronization at rest in the high gamma range (55-100 Hz) compared with controls and failed to show an increase in gamma synchronization during rest compared with the task, as observed in controls. Subgroup analysis revealed that pathological gamblers without a history of stimulant abuse had lower PCC power during the stop-signal task compared with controls and gamblers with previous stimulant abuse. Furthermore, gamblers with a history of stimulant abuse had up to four times higher power at the ACC site during rest and the task compared with controls. In conclusion, pathological gamblers had higher impulsivity and functional paralimbic abnormalities, which could not be explained by a history of stimulant abuse. In addition, previous stimulant abuse had a marked effect on the amplitude of oscillatory brain activity in the ACC and PCC, suggesting long-term deleterious effects of repeated dopaminergic drug exposure. These consequences should be investigated in more detail in longitudinal studies.coherence of consciousness | default mode | attention deficit hyperactivity disorder | borderline personality disorder

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Section: Discussionmentioning

confidence: 59%

Altered paralimbic interaction in behavioral addiction

Thomsen

Joensson

Lou

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…Previous studies from our group and others demonstrate a high degree of similarity between human and mouse EEG and ERPs for morphology, as well as physiological and pharmacological response properties using this configuration (Ehrlichman, Maxwell, Majumdar, & Siegel, 2008;Halene & Siegel, 2008;Rabin et al, 2008;Metzger, Maxwell, Liang, & Siegel, 2007;Phillips, Ehrlichman, & Siegel, 2007;Maxwell, Ehrlichman, Liang, Gettes, et al, 2006;Maxwell, Ehrlichman, Liang, Trief, et al, 2006;Siegel et al, 2003Siegel et al, , 2005Connolly et al, 2003Connolly et al, , 2004Maxwell, Kanes, Abel, & Siegel, 2004;Maxwell, Liang, et al, 2004;Umbricht et al, 2004;Umbricht, Latanov, Vissotksi, Nitsch, & Lipp, 2002;Stevens, Kem, & Freedman, 1999;Stevens, Kem, Mahnir, & Freedman, 1998;Stevens & Wear, 1997;Stevens et al, 1996;Stevens, Meltzer, & Rose, 1995). In animals, acute injection of ketamine similarly affects this ratio, as well as the magnitude and latency of the ERP components Maxwell, Ehrlichman, Liang, Trief, et al, 2006;Connolly et al, 2003Connolly et al, , 2004.…”

Section: Introductionmentioning

confidence: 54%

Ketamine Modulates Theta and Gamma Oscillations

Lazarewicz¹,

Ehrlichman²,

Maxwell³

et al. 2010

Journal of Cognitive Neuroscience

196

163

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Ketamine, an N-methyl-D-aspartate (NMDA) receptor glutamatergic antagonist, has been studied as a model of schizophrenia when applied in subanesthetic doses. In EEG studies, ketamine affects sensory gating and alters the oscillatory characteristics of neuronal signals in a complexmanner. We investigated the effects of ketamine on in vivo recordings from the CA3 region of mouse hippocampus referenced to the ipsilateral frontal sinus using a paired-click auditory gating paradigm. One issue of particular interest was elucidating the effect of ketamine on background network activity, poststimulus evoked and induced activity. We find that ketamine attenuates the theta frequency band in both background activity and in poststimulus evoked activity. Ketamine also disrupts a late, poststimulus theta power reduction seen in control recordings. In the gamma frequency range, ketamine enhances both background and evoked power, but decreases relative induced power. These findings support a role for NMDA receptors in mediating the balance between theta and gamma responses to sensory stimuli, with possible implications for dysfunction in schizophrenia. In EEG studies, ketamine affects sensory gating and alters the oscillatory characteristics of neuronal signals in a complex manner. We investigated the effects of ketamine on in vivo recordings from the CA3 region of mouse hippocampus referenced to the ipsilateral frontal sinus using a paired-click auditory gating paradigm. One issue of particular interest was elucidating the effect of ketamine on background network activity, poststimulus evoked and induced activity. We find that ketamine attenuates the theta frequency band in both background activity and in poststimulus evoked activity. Ketamine also disrupts a late, poststimulus theta power reduction seen in control recordings. In the gamma frequency range, ketamine enhances both background and evoked power, but decreases relative induced power. These findings support a role for NMDA receptors in mediating the balance between theta and gamma responses to sensory stimuli, with possible implications for dysfunction in schizophrenia. ■ Disciplines Physical Sciences and Mathematics | Physics

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“…Nicotine may also have diverse actions across two measures of auditory gating in mice, in that it can increase the amplitude and the gating of the P20 evoked potentials whereas it may decrease that of N40 evoked potential (Metzger et al, 2007). The enhancing effects of nicotine on P20 auditory evoked potential in mice was confirmed in another study where it was also verified that the actions of nicotine could be blocked by mecamylamine (Phillips et al, 2007), suggesting involvement of nicotinic receptors in this action of nicotine. Thus, the effect of nicotine may vary depending on the paradigm and the species used.…”

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confidence: 84%

Nicotine and nicotinic system in hypoglutamatergic models of schizophrenia

Tizabi

2007

neurotox res

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Schizophrenia is a complex neuropsychiatric disorder with devastating consequences. It is characterized by thought fragmentation, hallucination and delusion, collectively referred to as positive symptoms. In addition, mood changes or affective disorders, referred to as negative symptoms, as well as cognitive impairments can be manifested in these patients. Arguably, modeling such a disorder in its entirety in animals might not be feasible. Despite this limitation, various models with significant construct, predictive and some face validity have been developed. One such model, based on hypoglutamatergic hypothesis of schizophrenia, makes use of administering NMDA receptor antagonists and evaluating behavioral paradigms such as sensorimotor gating. Because of very high incidence of smoking among schizophrenic patients, it has been postulated that some of these patients may actually be self medicating with tobacco's nicotine. Research on nicotinic-glutamatergic interactions using various animal models has yielded conflicting results. In this review, some of these models and possible confounding factors are discussed. Overall, a therapeutic potential for nicotinic agonists in schizophrenia can be suggested. Moreover, it is evident that various experimental paradigms or models of schizophrenia symptoms need to be combined to provide a wider spectrum of the behavioral phenotype, as each model has its inherent limitations.

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Mecamylamine blocks nicotine-induced enhancement of the P20 auditory event–related potential and evoked gamma

Cited by 49 publications

References 59 publications

Altered paralimbic interaction in behavioral addiction

Altered paralimbic interaction in behavioral addiction

Ketamine Modulates Theta and Gamma Oscillations

Nicotine and nicotinic system in hypoglutamatergic models of schizophrenia

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