Endocannabinoid–Dopamine Interactions in Striatal Synaptic Plasticity

Mathur, Brian N.; Lovinger, David M.

doi:10.3389/fphar.2012.00066

Cited by 68 publications

(81 citation statements)

References 120 publications

(210 reference statements)

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“…Also implicated in sensory gating are generators in the frontal lobe (Korzyukov et al, 2007;Weisser et al, 2001), superior temporal gyrus (Thoma et al, 2005), prefrontal cortex (Grunwald et al, 2003), and cingulate and parietal lobe regions (Boutros et al, 2013), along with multiple neurotransmitter systems including GABAergic, cholinergic, dopaminergic, serotonergic and glutamatergic systems (Adler et al, 1998). Relevant to the current study and as noted earlier, THC is thought to disrupt the regulatory action of the endocannabinoid system on these neurotransmitter systems (Lopez-Moreno et al, 2008;Mathur and Lovinger, 2012).…”

Section: Introductionsupporting

confidence: 60%

“…The subjective, behavioural and cognitive effects produced by THC are most likely due to the action of THC as a partial agonist at central cannabinoid (e.g. CB 1 ) receptor sites (Pertwee, 2008), altering the regulatory action of the endocannabinoid system on synaptic transmission and other neurotransmitter signalling, such as gamma-aminobutyric acid (GABA), glutamate and dopamine (Lopez-Moreno et al, 2008;Mathur and Lovinger, 2012). CB 1 receptors occur in high density throughout the brain, particularly in the hippocampus, anterior cingulate, basal ganglia and the cerebellum; regions which are involved in cognition and are particularly important for attention, learning and memory (Bhattacharyya et al, 2009;Bossong and Niesink, 2010;Iversen, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Chronic effects of cannabis on sensory gating

Broyd

Greenwood

Croft

et al. 2013

International Journal of Psychophysiology

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Chronic cannabis use has been associated with neurocognitive deficits, alterations in brain structure and function, and with psychosis. This study investigated the effects of chronic cannabis use on P50 sensory-gating in regular users, and explored the association between sensory gating, cannabis use history and the development of psychotic-like symptoms. Twenty controls and 21 regular cannabis users completed a P50 paired-click (S1 and S2) paradigm with an inter-pair interval of 9. s. The groups were compared on P50 amplitude to S1 and S2, P50 ratio (S2/S1) and P50 difference score (S1-S2). While cannabis users overall did not differ from controls on P50 measures, prolonged duration of regular use was associated with greater impairment in sensory gating as indexed by both P50 ratio and difference scores (including after controlling for tobacco use). Long-term cannabis users were found to have worse sensory gating ratios and difference scores compared to short-term users and controls. P50 metrics did not correlate significantly with any measure of psychotic-like symptoms in cannabis users. These results suggest that prolonged exposure to cannabis results in impaired P50 sensory-gating in long-term cannabis users. While it is possible that these deficits may have pre-dated cannabis use and reflect a vulnerability to cannabis use, their association with increasing years of cannabis use suggests that this is not the case. Impaired P50 sensory-gating ratios have also been reported in patients with schizophrenia and may indicate a similar underlying pathology.

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Section: Introductionsupporting

confidence: 60%

Section: Introductionmentioning

confidence: 99%

Chronic effects of cannabis on sensory gating

Broyd

Greenwood

Croft

et al. 2013

International Journal of Psychophysiology

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“…Particularly important among them are questions about the roles that other modulatory neurotransmitters may play in regulating the interaction between oxytocin and anandamide. Previous studies point toward serotonin, which is needed for the expression of oxytocin-dependent plasticity in the NAc (12), and dopamine, which has been implicated in striatal anandamide signaling (30,31). Defining such roles will require, however, further investigation.…”

Section: Discussionmentioning

confidence: 99%

Endocannabinoid signaling mediates oxytocin-driven social reward

Don

Lee

Cox

et al. 2015

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

183

160

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Marijuana exerts profound effects on human social behavior, but the neural substrates underlying such effects are unknown. Here we report that social contact increases, whereas isolation decreases, the mobilization of the endogenous marijuana-like neurotransmitter, anandamide, in the mouse nucleus accumbens (NAc), a brain structure that regulates motivated behavior. Pharmacological and genetic experiments show that anandamide mobilization and consequent activation of CB 1 cannabinoid receptors are necessary and sufficient to express the rewarding properties of social interactions, assessed using a socially conditioned place preference test. We further show that oxytocin, a neuropeptide that reinforces parental and social bonding, drives anandamide mobilization in the NAc. Pharmacological blockade of oxytocin receptors stops this response, whereas chemogenetic, site-selective activation of oxytocin neurons in the paraventricular nucleus of the hypothalamus stimulates it. Genetic or pharmacological interruption of anandamide degradation offsets the effects of oxytocin receptor blockade on both social place preference and cFos expression in the NAc. The results indicate that anandamidemediated signaling at CB 1 receptors, driven by oxytocin, controls social reward. Deficits in this signaling mechanism may contribute to social impairment in autism spectrum disorders and might offer an avenue to treat these conditions. endocannabinoid | oxytocin | reward | social behavior | anandamide

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“…by alterations in retrograde endocannabinoid signaling or other mechanisms (110). Such alterations may well contribute to the described behavioral deficits.…”

Section: Behavioural Consequences Of Altered Striatal Circuit Functiomentioning

confidence: 99%

Insights About Striatal Circuit Function and Schizophrenia From a Mouse Model of Dopamine D2 Receptor Upregulation

Simpson

Kellendonk

2017

Biological Psychiatry

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The dopamine hypothesis of schizophrenia is supported by a large number of imaging studies that have identified an increase in dopamine binding at the D2 receptor selectively in the striatum. Here we review a decade of work using a regionally restricted and temporally regulated transgenic mouse model to investigate the behavioral, molecular, electrophysiological, and anatomical consequences of selective D2 receptor upregulation in the striatum. These studies have identified new and potentially important biomarkers at the circuit and molecular level that can now be explored in patients with schizophrenia. They provide an example of how animal models and their detailed level of neurobiological analysis allow a deepening of our understanding of the relationship between neuronal circuit function and symptoms of schizophrenia, and as a consequence generate new hypotheses that are testable in patients.

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Endocannabinoid–Dopamine Interactions in Striatal Synaptic Plasticity

Cited by 68 publications

References 120 publications

Chronic effects of cannabis on sensory gating

Chronic effects of cannabis on sensory gating

Endocannabinoid signaling mediates oxytocin-driven social reward

Insights About Striatal Circuit Function and Schizophrenia From a Mouse Model of Dopamine D2 Receptor Upregulation

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