Sensory gating, Cannabinoids and Schizophrenia

Dissanayake, Dilshani W. N.; Mason, Robert J.; Marsden, C.A.

doi:10.1016/j.neuropharm.2012.10.011

Cited by 28 publications

(17 citation statements)

References 158 publications

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“…In patients, this is thought to be an impairment of auditory sensory memory and has been found to be related to the duration (Umbricht and Krljes, 2005) and the genetic aspect (Näätänen and Kähkönen, 2009) of the illness. Our findings add to the growing literature on ERP measures, including the P50, an index of sensory gating (Dissanayake et al, 2013) and the P300, an index of attention/novelty detection (Gallinat et al, 2012;Roser et al, 2008aRoser et al, , 2008b, as well as behavioral tasks of perception and attention (Solowij and Michie, 2007), which suggest that habitual cannabis use can negatively impact elementary sensory and early attentional processes, which are frequently impaired in SZ. Although cannabis use is neither a necessary nor sufficient cause of psychotic illness, our results also show some support for the "component cause" hypothesis, whereby heavy cannabis use in early adolescence is thought to induce SZ-like cognitive symptoms (Sewell et al, 2010).…”

Section: Discussionsupporting

confidence: 67%

Mismatch negativity in tobacco-naïve cannabis users and its alteration with acute nicotine administration

Impey

El-Marj

Parks

et al. 2015

Pharmacology Biochemistry and Behavior

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Section: Discussionsupporting

confidence: 67%

Mismatch negativity in tobacco-naïve cannabis users and its alteration with acute nicotine administration

Impey

El-Marj

Parks

et al. 2015

Pharmacology Biochemistry and Behavior

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“…The precise mechanisms by which prolonged exposure to cannabis might alter the neuronal substrates which underpin P50 indices of sensory gating remain unclear [ 61 ]. The generators of the P50 evoked potential have been localised to Heschl's gyrus in the primary auditory cortex [ 62 – 64 ].…”

Section: Discussionmentioning

confidence: 99%

Mismatch Negativity and P50 Sensory Gating in Abstinent Former Cannabis Users

et al. 2016

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Prolonged heavy exposure to cannabis is associated with impaired cognition and brain functional and structural alterations. We recently reported attenuated mismatch negativity (MMN) and altered P50 sensory gating in chronic cannabis users. This study investigated the extent of brain functional recovery (indexed by MMN and P50) in chronic users after cessation of use. Eighteen ex-users (median 13.5 years prior regular use; median 3.5 years abstinence) and 18 nonusers completed (1) a multifeature oddball task with duration, frequency, and intensity deviants and (2) a P50 paired-click paradigm. Trend level smaller duration MMN amplitude and larger P50 ratios (indicative of poorer sensory gating) were observed in ex-users compared to controls. Poorer P50 gating correlated with prior duration of cannabis use. Duration of abstinence was positively correlated with duration MMN amplitude, even after controlling for age and duration of cannabis use. Impaired sensory gating and attenuated MMN amplitude tended to persist in ex-users after prolonged cessation of use, suggesting a lack of full recovery. An association with prolonged duration of prior cannabis use may indicate persistent cannabis-related alterations to P50 sensory gating. Greater reductions in MMN amplitude with increasing abstinence (positive correlation) may be related to either self-medication or an accelerated aging process.

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“…High densities of CB 1 receptors have been found in brain areas that regulate sensorimotor gating such as prefrontal cortex, amygdala and hippocampus (Dissanayake et al, 2013). Moreover, CB 1 receptors have a modulatory role on specific neurotransmitter systems, mainly glutamate, GABA and dopamine (Schlicker and Kathmann, 2001), which have a critical role in the PPI processing.…”

Section: Discussionmentioning

confidence: 99%

Effects of cannabinoid drugs on the deficit of prepulse inhibition of startle in an animal model of schizophrenia: the SHR strain

et al. 2014

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Clinical and neurobiological findings suggest that the cannabinoids and the endocannabinoid system may be implicated in the pathophysiology and treatment of schizophrenia. We described that the spontaneously hypertensive rats (SHR) strain presents a schizophrenia behavioral phenotype that is specifically attenuated by antipsychotic drugs, and potentiated by proschizophrenia manipulations. Based on these findings, we have suggested this strain as an animal model of schizophrenia. The aim of this study was to evaluate the effects of cannabinoid drugs on the deficit of prepulse inhibition (PPI) of startle, the main paradigm used to study sensorimotor gating impairment related to schizophrenia, presented by the SHR strain. The following drugs were used: (1) WIN55212,2 (cannabinoid agonist), (2) rimonabant (CB1 antagonist), (3) AM404 (anandamide uptake inhibitor), and (4) cannabidiol (CBD; indirect CB1/CB2 receptor antagonist, among other effects). Wistar rats (WRs) and SHRs were treated with vehicle (VEH) or different doses of WIN55212 (0.3, 1, or 3 mg/kg), rimonabant (0.75, 1.5, or 3 mg/kg), AM404 (1, 5, or 10 mg/kg), or CBD (15, 30, or 60 mg/kg). VEH-treated SHRs showed a decreased PPI when compared to WRs. This PPI deficit was reversed by 1 mg/kg WIN and 30 mg/kg CBD. Conversely, 0.75 mg/kg rimonabant decreased PPI in SHR strain, whereas AM404 did not modify it. Our results reinforce the role of the endocannabinoid system in the sensorimotor gating impairment related to schizophrenia, and point to cannabinoid drugs as potential therapeutic strategies.

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Sensory gating, Cannabinoids and Schizophrenia

Cited by 28 publications

References 158 publications

Mismatch negativity in tobacco-naïve cannabis users and its alteration with acute nicotine administration

Mismatch negativity in tobacco-naïve cannabis users and its alteration with acute nicotine administration

Mismatch Negativity and P50 Sensory Gating in Abstinent Former Cannabis Users

Effects of cannabinoid drugs on the deficit of prepulse inhibition of startle in an animal model of schizophrenia: the SHR strain

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