Modulation of transmitter release via presynaptic cannabinoid receptors

Schlicker, Eberhard; Kathmann, M.

doi:10.1016/s0165-6147(00)01805-8

Cited by 596 publications

(349 citation statements)

References 76 publications

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“…[18][19][20][21][22] This cellular MOA is also consistent with the molecular distinction between agonist and inverse agonist. Although most comparisons of agonists to inverse agonists are on the basis of recombinant expression systems, ex vivo assays of brain slice electrophysiology have indicated that rimonabant's effect is consistent with an inverse agonist effect under these conditions, in which the likelihood of endocannabinoid release is low.…”

Section: Molecular and Cellular Moasupporting

confidence: 81%

Cannabinoid-1 receptor inverse agonists: current understanding of mechanism of action and unanswered questions

Fong

Heymsfield

2009

Int J Obes

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Rimonabant and taranabant are two extensively studied cannabinoid-1 receptor (CB1R) inverse agonists. Their effects on in vivo peripheral tissue metabolism are generally well replicated. The central nervous system site of action of taranabant or rimonabant is firmly established based on brain receptor occupancy studies. At the whole-body level, the mechanism of action of CB1R inverse agonists includes a reduction in food intake and an increase in energy expenditure. At the tissue level, fat mass reduction, liver lipid reduction and improved insulin sensitivity have been shown. These effects on tissue metabolism are readily explained by CB1R inverse agonist acting on brain CB1R and indirectly influencing the tissue metabolism through the autonomic nervous system. It has also been hypothesized that rimonabant acts directly on adipocytes, hepatocytes, pancreatic islets or skeletal muscle in addition to acting on brain CB1R, although strong support for the contribution of peripherally located CB1R to in vivo efficacy is still lacking. This review will carefully examine the published literature and provide a perspective on what new tools and studies are required to address the peripheral site of action hypothesis.

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Section: Molecular and Cellular Moasupporting

confidence: 81%

Cannabinoid-1 receptor inverse agonists: current understanding of mechanism of action and unanswered questions

Fong

Heymsfield

2009

Int J Obes

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“…In addition, it has been shown that the cannabinoid system affects the hippocampal LTP by chronic D 9 -THC blocking hippocampal LTP via CB 1 receptors after withdrawal (Hoffman et al, 2007). It has been shown that cannabinoids inhibit neurotransmitter release via presynaptic cannabinoid CB 1 receptors (Schlicker and Kathmann, 2001). Additionally, LTP disruption in the hippocampus by WIN 55,212-2 may be associated with an inhibition of hippocampal glutamatergic transmission (Misner and Sullivan, 1999).…”

Section: Discussionmentioning

confidence: 99%

A Cannabinoid CB1 Receptor Antagonist Ameliorates Impairment of Recognition Memory on Withdrawal from MDMA (Ecstasy)

Nawata

Hiranita

Yamamoto

2009

Neuropsychopharmacol

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( + /À)-3,4-Methylenedioxymethamphetamine (MDMA, 'Ecstasy') abusers have persistent neuropsychiatric deficits including memory impairments after the cessation of abuse. On the other hand, cannabinoid CB 1 receptors have been implicated in learning/memory, and are highly expressed in the hippocampus, a region of the brain believed to have an important function in certain forms of learning and memory. In this study, we clarified the mechanism underlying the cognitive impairment that develops during MDMA withdrawal from the standpoint of the cannabinoid CB 1 receptors. Mice were administered MDMA (10 mg/kg, i.p.) once a day for 7 days. On the 7th day of withdrawal, a novel object recognition task was performed and the amount of cannabinoid CB 1 receptor protein was measured with western blotting. Recognition performance was impaired on the 7th day of withdrawal. This impairment was blocked by AM251, a cannabinoid CB 1 receptor antagonist, administered 30 min before the training trial or co-administered with MDMA. At this time, the level of cannabinoid CB 1 receptor protein increased significantly in the hippocampus but not the prefrontal cortex or striatum. This increase of CB 1 receptor protein in the hippocampus was also blocked by the co-administration of AM251. Furthermore, CB 1 receptor knockout mice showed no impairment of recognition performance on the withdrawal from MDMA. The impairment of recognition memory during withdrawal from MDMA may result from the activation of cannabinoid CB 1 receptors in the hippocampus.

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“…The existing literature on presynaptic effects of cannabinoids indicates that virtually every step in the process leading to vesicle release is a potential site of action for cannabinoids. These mechanisms have been extensively described in recent reviews (Ameri, 1999;Schlicker & Kathmann, 2001;Howlett et al, 2002) and are only briefly recalled hereafter. Each of these modes of operation has already been suggested for brain areas where CB1Rs are functional, although with distinct specificities from region to region:…”

Section: Potential Sites Of Action Of Endocannabinoidsmentioning

confidence: 99%

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

Diana

Marty

2004

British J Pharmacology

230

168

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Depolarization-induced suppression of inhibition (DSI) and depolarization-induced suppression of excitation (DSE) are two related forms of short-term synaptic plasticity of GABAergic and glutamatergic transmission, respectively. They are induced by calcium concentration increases in postsynaptic cells and are mediated by the release of a retrograde messenger, which reversibly inhibits afferent synapses via presynaptic mechanisms. We review here:(1) The evidence accumulated during the 1990s that has led to the conclusion that DSI/DSE rely on retrograde signaling. (2) The more recent research that has led to the identification of endocannabinoids as the retrograde messengers responsible for DSI/DSE. (3) The possible mechanisms by which presynaptic type 1 cannabinoid receptors reduce synaptic efficacy during DSI/DSE. (4) The possible modes of induction of DSI/DSE by physiological activity patterns, and the partially conflicting evaluations of the calcium concentration increases required for cannabinoid synthesis. (5) Finally, the relation between DSI/DSE and other forms of long-and short-term synaptic inhibition, which were more recently associated with the production of endocannabinoids by postsynaptic cells.We conclude that recent studies on DSI/DSE have uncovered a specific and original mode of action for endocannabinoids in the brain, and that they have opened new avenues to understand the role of retrograde signaling in central synapses.

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Modulation of transmitter release via presynaptic cannabinoid receptors

Cited by 596 publications

References 76 publications

Cannabinoid-1 receptor inverse agonists: current understanding of mechanism of action and unanswered questions

Cannabinoid-1 receptor inverse agonists: current understanding of mechanism of action and unanswered questions

A Cannabinoid CB1 Receptor Antagonist Ameliorates Impairment of Recognition Memory on Withdrawal from MDMA (Ecstasy)

Endocannabinoid‐mediated short‐term synaptic plasticity: depolarization‐induced suppression of inhibition (DSI) and depolarization‐induced suppression of excitation (DSE)

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