Differential effects of chronic cannabis use on preattentional cognitive functioning in abstinent schizophrenic patients and healthy subjects

Rentzsch, Johannes; Buntebart, Elise; Stadelmeier, Ada; Gallinat, Jürgen; Jockers-Scherübl, Maria C.

doi:10.1016/j.schres.2011.05.011

Cited by 29 publications

(42 citation statements)

References 52 publications

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“…General evidence for a different pattern of neurophysiological expression in the MMN component was found for psychosis patients who used cannabis compared to those that did not. Cannabis use did not significantly increase MMN amplitude; however, similar to Rentzsch et al (2011), a relatively consistent pattern emerged across groups for MMN peak amplitude, with patients who used cannabis appearing to lie intermediate between controls (who showed the highest MMN amplitude) and patients who did not use cannabis (who showed the lowest MMN amplitude). These findings parallel neuropsychological findings in the literature, where cannabis-using patients show 'superior' neuropsychological functioning compared to non-using patients (Stirling et al 2005;Jockers-Scherübl et al 2007;de la Serna et al 2010;Yücel et al 2012).…”

Section: Discussionsupporting

confidence: 50%

“…Most recently, this research group reported that acute administration of subanaesthetic doses of ketamine to healthy volunteers did not affect frequency or duration MMN amplitudes, but coadministration of the cannabinoid receptor antagonist rimonabant resulted in frontally reduced duration MMN (Roser et al 2011). Finally, reduced frontal frequency MMN was reported in long-term cannabis users relative to controls (Rentzsch et al 2011). This study also included schizophrenia patients with and without cannabis use and found increased frontal MMN in the former relative to the latter, and MMN amplitude in the cannabis-using patients did not differ significantly from controls.…”

Section: Introductionmentioning

confidence: 98%

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Delayed preattentional functioning in early psychosis patients with cannabis use

et al. 2012

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Section: Discussionsupporting

confidence: 50%

Section: Introductionmentioning

confidence: 98%

Delayed preattentional functioning in early psychosis patients with cannabis use

et al. 2012

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“…One explanation for this finding might be that processing of sound duration deviants is affected to a larger degree than the processing of sound frequency deviants in PD patients. This explanation is supported by studies showing divergent deficits in duration and frequency MMN amplitudes in other psychiatric conditions [57, 58], likely due to differences in the underlying neuronal networks involved in preattentive deviant sound processing. While frequency deviants seem to be processed in auditory-temporal brain areas, duration deviant processing seems to involve further key brain areas forming greater and more distributed networks [59].…”

Section: Discussionmentioning

confidence: 67%

Reduced Sensitivity to Non-Fear-Related Stimulus Changes in Panic Disorder

et al. 2019

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Panic disorder (PD) is associated with increased body vigilance and reduced cognitive resources directed at non-fear-related stimuli, particularly in the absence of stimulus-rich environments. To date, only few studies have investigated whether this deficit in PD is reflected in reduced mismatch negativity (MMN), an event-related potential indexing preattentive sensitivity to unexpected stimulus changes. We tested 35 patients affected by PD and 42 matched healthy controls in an oddball paradigm, using frequency and duration deviant stimuli to measure auditory MMN. PD patients displayed reduced duration MMN amplitudes in comparison to healthy controls. No group differences were detected for duration MMN latency, as well as frequency MMN indices. Results support the notion of reduced processing of non-fear-related stimuli in PD patients, particularly with regard to the preattentive processing of sound duration deviants. Additionally, our findings are in line with clinical studies reporting divergent deficits in preattentive processing of frequency and duration deviants.

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“…For example, although social withdrawal in PCP-treated rats is associated with reduced CB 1 activation, working memory deficits in the same animals have been linked to increased activity at CB 1 receptors (Seillier et al, 2010). In addition, alterations of endocannabinoid transmission in control animals via URB597, AM251, or chronic WIN55,212-2 (Spano et al, 2010) produced deleterious effects similar to those observed in PCP-treated rats, suggesting that cannabinoid drugs trigger different behavioral responses in distinct experimental groups, as in the case of schizophrenics vs healthy subjects (Rentzsch et al, 2011). Finally, chronic cannabis consumption has been shown to attenuate negative symptoms in the former group (Compton et al, 2004;Dubertret et al, 2006), but to induce an 'amotivational syndrome' in the latter (Sewell et al, 2009).…”

Section: Discussionmentioning

confidence: 97%

Phencyclidine-Induced Social Withdrawal Results from Deficient Stimulation of Cannabinoid CB1 Receptors: Implications for Schizophrenia

Seillier

Bahillo

Giuffrida

2013

Neuropsychopharmacol

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The neuronal mechanisms underlying social withdrawal, one of the core negative symptoms of schizophrenia, are not well understood. Recent studies suggest an involvement of the endocannabinoid system in the pathophysiology of schizophrenia and, in particular, of negative symptoms. We used biochemical, pharmacological, and behavioral approaches to investigate the role played by the endocannabinoid system in social withdrawal induced by sub-chronic administration of phencyclidine (PCP). Pharmacological enhancement of endocannabinoid levels via systemic administration of URB597, an inhibitor of endocannabinoid degradation, reversed social withdrawal in PCP-treated rats via stimulation of CB 1 receptors, but reduced social interaction in control animals through activation of a cannabinoid/vanilloid-sensitive receptor. In addition, the potent CB agonist CP55,940 reversed PCP-induced social withdrawal in a CB 1 -dependent manner, whereas pharmacological blockade of CB 1 receptors by either AM251 or SR141716 reduced the time spent in social interaction in control animals. PCP-induced social withdrawal was accompanied by a decrease of anandamide (AEA) levels in the amygdala and prefrontal cortex, and these deficits were reversed by URB597. As CB 1 receptors are predominantly expressed on GABAergic interneurons containing the anxiogenic peptide cholecystokinin (CCK), we also examined whether the PCP-induced social withdrawal resulted from deficient CB 1 -mediated modulation of CCK transmission. The selective CCK2 antagonist LY225910 blocked both PCP-and AM251-induced social withdrawal, but not URB597 effect in control rats. Taken together, these findings indicate that AEA-mediated activation of CB 1 receptors is crucial for social interaction, and that PCP-induced social withdrawal results from deficient endocannabinoid transmission.

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Differential effects of chronic cannabis use on preattentional cognitive functioning in abstinent schizophrenic patients and healthy subjects

Cited by 29 publications

References 52 publications

Delayed preattentional functioning in early psychosis patients with cannabis use

Delayed preattentional functioning in early psychosis patients with cannabis use

Reduced Sensitivity to Non-Fear-Related Stimulus Changes in Panic Disorder

Phencyclidine-Induced Social Withdrawal Results from Deficient Stimulation of Cannabinoid CB1 Receptors: Implications for Schizophrenia

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