Neurochemical evidence that stimulation of CB1 cannabinoid receptors on GABAergic nerve terminals activates the dopaminergic reward system by increasing dopamine release in the rat nucleus accumbens

Sperlágh, Beáta; Windisch, K.; Andó, Rómeó D.; Vizi, E. Sylvester

doi:10.1016/j.neuint.2009.01.017

Cited by 61 publications

(31 citation statements)

References 54 publications

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“…Intracerebroventricular administration of N/OFQ in rats inhibits dopamine release from the nucleus accumbens (Murphy et al 1996) and decreases morphine-and cocaineinduced release of dopamine in the same nucleus (Di Giannuario et al 1999;Lutfy et al 2001). Conversely, CB1 receptor activation causes an increase of dopamine release in the nucleus accumbens via a GABAergic pathway (Sperlágh et al 2009). …”

Section: Discussionmentioning

confidence: 99%

∆9-Tetrahydrocannabinol Decreases NOP Receptor Density and mRNA Levels in Human SH-SY5Y Cells

et al. 2011

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Several studies demonstrated a cross-talk between the opioid and cannabinoid system. The NOP receptor and its endogenous ligand nociceptin/orphanin FQ represent an opioid-related functional entity that mediates some non-classical opioid effects. The relationship between cannabinoid and nociceptin/NOP system is yet poorly explored. In this study, we used the neuroblastoma SH-SY5Y cell line to investigate the effect of delta-9-tetrahydrocannabinol (∆(9)-THC) on nociceptin/NOP system. Results revealed that the exposure to ∆(9)-THC (100, 150, and 200 nM) for 24 h produces a dose-dependent NOP receptor B (max) down-regulation. Moreover, ∆(9)-THC caused a dose-dependent decrease in NOP mRNA levels. The selective cannabinoid receptor CB1 antagonist AM251 (1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-1-piperidinyl-1H-pyrazole-3-carboxamide) reduces both effects, suggesting that ∆(9)-THC activation of CB1 receptor is involved in the observed effects. These data show evidence of a cross-talk between NOP and CB1 receptors, thus suggesting a possible interplay between cannabinoid and nociceptin/NOP system.

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Section: Discussionmentioning

confidence: 99%

∆9-Tetrahydrocannabinol Decreases NOP Receptor Density and mRNA Levels in Human SH-SY5Y Cells

et al. 2011

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“…For example, the acute administration of THC has been reported to increase levels of β-endorphins and enkephalinergic peptides directly in the mesolimbic DA pathway, including the VTA and NAcc (68). Acute THC also increases the reinforcing efficacy of intravenously administered heroin (69) facilitates the release of DA from NAc DAergic terminals (70, 71) and directly activates VTA DA neurons recorded in vivo (72). In rat neurodevelopmental models, adolescent THC exposure has been reported to strongly increase opiate self-administration in early adulthood (73) and potentiate mesolimbic DA release (74).…”

Section: Cannabinoid Cb1 Receptor-mediated Modulation Of Reward Procementioning

confidence: 99%

The Role of Cannabinoid Transmission in Emotional Memory Formation: Implications for Addiction and Schizophrenia

et al. 2014

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Emerging evidence from both basic and clinical research demonstrates an important role for endocannabinoid (ECB) signaling in the processing of emotionally salient information, learning, and memory. Cannabinoid transmission within neural circuits involved in emotional processing has been shown to modulate the acquisition, recall, and extinction of emotionally salient memories and importantly, can strongly modulate the emotional salience of incoming sensory information. Two neural regions in particular, the medial prefrontal cortex (PFC) and the basolateral nucleus of the amygdala (BLA), play important roles in emotional regulation and contain high levels of cannabinoid receptors. Furthermore, both regions show profound abnormalities in neuropsychiatric disorders such as addiction and schizophrenia. Considerable evidence has demonstrated that cannabinoid transmission functionally interacts with dopamine (DA), a neurotransmitter system that is of exceptional importance for both addictive behaviors and the neuropsychopathology of disorders like schizophrenia. Research in our laboratory has focused on how cannabinoid transmission both within and extrinsic to the mesolimbic DA system, including the BLA → mPFC circuitry, can modulate both rewarding and aversive emotional information. In this review, we will summarize clinical and basic neuroscience research demonstrating the importance of cannabinoid signaling within this neural circuitry. In particular, evidence will be reviewed emphasizing the importance of cannabinoid signaling within the BLA → mPFC circuitry in the context of emotional salience processing, memory formation and memory-related plasticity. We propose that aberrant states of hyper or hypoactive ECB signaling within the amygdala-prefrontal cortical circuit may lead to dysregulation of mesocorticolimbic DA transmission controlling the processing of emotionally salient information. These disturbances may in turn lead to emotional processing, learning, and memory abnormalities related to various neuropsychiatric disorders, including addiction and schizophrenia-related psychoses.

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“…The endocannabinoid (EC) system is generally viewed as a neuromodulatory system that interacts with, and regulates the functions of several neurotransmitter systems, including the dopaminergic (DA), cholinergic, serotoninergic, adrenergic, opiate, glutamatergic and GABAergic systems (Freund et al, 2003; Sperlágh et al, 2009). By way of retrograde signaling, endocannabinoids provide essential feedback to limit neurotransmitter release from presynaptic terminals (Bacci et al, 2004; Marinelli et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

[125I]SD-7015 reveals fine modalities of CB1 cannabinoid receptor density in the prefrontal cortex during progression of Alzheimer’s disease

Farkas

Nagy

Palkovits

et al. 2012

Neurochemistry International

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The cannabinoid type-1 receptor (CB1R) is one of the most abundant members of the G protein-coupled receptor family in the central nervous system. Once activated by their cognate ligands, endocannabinoids, CB1Rs generally limit the timing of neurotransmitter release at many cortical synapses. Prior studies have indicated the involvement of CB1R in neurodegeneration and in various neuronal insults, with an emphasis on their neuroprotective role. In the present study we used a novel selective CB1R radioligand to investigate regional variations in CB1R ligand binding as a factor of progressive Braak tau pathology in the frontal cortex of Alzheimer's disease (AD) patients. The frontal cortex was chosen for this study due to the high density of CB1Rs and their well-characterized involvement in the progression of AD. Post-mortem prefrontal cortex samples from AD patients from Braak stages I to VI and controls were subjected to CB1R autoradiography with [125I]SD-7015 as radioligand. Regional concentration of [125I]SD-7015, corresponding to, and thereby representing, regional CB1R densities, were expressed in fM/g_tissue. The results show that CB1R density inversely correlates with Braak tau pathology with the following tendency: controls

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Neurochemical evidence that stimulation of CB1 cannabinoid receptors on GABAergic nerve terminals activates the dopaminergic reward system by increasing dopamine release in the rat nucleus accumbens

Cited by 61 publications

References 54 publications

∆9-Tetrahydrocannabinol Decreases NOP Receptor Density and mRNA Levels in Human SH-SY5Y Cells

∆9-Tetrahydrocannabinol Decreases NOP Receptor Density and mRNA Levels in Human SH-SY5Y Cells

The Role of Cannabinoid Transmission in Emotional Memory Formation: Implications for Addiction and Schizophrenia

[125I]SD-7015 reveals fine modalities of CB1 cannabinoid receptor density in the prefrontal cortex during progression of Alzheimer’s disease

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