The CB1 receptor antagonist, SR141716A, prevents high-frequency stimulation-induced reduction of feedback inhibition in the rat dentate gyrus following perforant path stimulation in vivo

Sokal, David M.; Benetti, Carla da Silva; Girlanda, Elena; Large, Charles H.

doi:10.1016/j.brainres.2008.05.065

Cited by 7 publications

(5 citation statements)

References 29 publications

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“…De Oliveira Alvares et al (2006) have demonstrated impairment of LTP in a CA1 slice preparation following AM251 administration. Sokal et al (2008) found that the CB1 receptor antagonist SR141716A blocked the potentiation of the fEPSP slope observed following HFS to the perforant path. However, other studies conducted on hippocampal slices of the Schaffer collateral-CA1 synapses have shown that CB1 blockade favors LTP in the hippocampus (Slanina et al, 2005) and that mice lacking CB1 receptors show enhanced LTP (Bohme et al, 2000).…”

Section: The Involvement Of the Cannabinoid System In Hippocampal Ltpmentioning

confidence: 97%

Cannabinoids modulate hippocampal memory and plasticity

2009

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Considerable evidence demonstrates that cannabinoid agonists impair whereas cannabinoid antagonists improve memory and plasticity. However, recent studies suggest that the effects of cannabinoids on learning do not necessarily follow these simple patterns, particularly when emotional memory processes are involved. We investigated the involvement of the cannabinoid system in hippocampal learning and plasticity using the fear-related inhibitory avoidance (IA) and the non-fear-related spatial learning paradigms, and cellular models of learning and memory, i.e., long-term potentiation (LTP) and long-term depression (LTD). We found that microinjection into the CA1 of the CB1/CB2 receptor agonist WIN55,212-2 (5 μg/side) and an inhibitor of endocannabinoid reuptake and breakdown AM404 (200 ng/side) facilitated the extinction of IA, while the CB1 receptor antagonist AM251 (6 ng/side) impaired it. WIN55,212-2 and AM251 did not affect IA conditioning, while AM404 enhanced it, probably due to a drug-induced increase in pain sensitivity. However, in the water maze, systemic or local CA1 injections of AM251, WIN55,212-2, and AM404 all impaired spatial learning. We also found that i.p. administration of WIN55,212-2 (0.5 mg/kg), AM404 (10 mg/kg), and AM251 (2 mg/kg) impaired LTP in the Schaffer collateral-CA1 projection, whereas AM404 facilitated LTD. Our findings suggest diverse effects of the cannabinoid system on CA1 memory and plasticity that cannot be categorized simply into an impairing or an enhancing effect of cannabinoid activation and deactivation, respectively. Moreover, they provide preclinical support for the suggestion that targeting the endocannabinoid system may aid in the treatment of disorders associated with impaired extinction-like processes, such as post-traumatic stress disorder.

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Section: The Involvement Of the Cannabinoid System In Hippocampal Ltpmentioning

confidence: 97%

Cannabinoids modulate hippocampal memory and plasticity

2009

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“…Exogenously applied cannabinoid agonists (WIN55212‐2 and Δ 9 ‐THC), as well as endocannabinoid degradation inhibitors, block the induction of LTP (Carlson et al ., 2002; Slanina and Schweitzer, 2005; Hoffman et al ., 2007; Abush and Akirav, 2010). Administration of AM251 (de Oliveira et al ., 2006) or rimonabant (Sokal et al ., 2008) also blocks the induction of LTP, interpreted as the blockade of endocannabinoid influence on GABAergic neurons (Abush and Akirav, 2010).…”

Section: Neurophysiological Responses That Can Be Attributed To Tonicmentioning

confidence: 99%

Endocannabinoid tone versus constitutive activity of cannabinoid receptors

Howlett

Reggio

Childers

et al. 2011

British J Pharmacology

109

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This review evaluates the cellular mechanisms of constitutive activity of the cannabinoid (CB) receptors, its reversal by inverse agonists, and discusses the pitfalls and problems in the interpretation of the research data. The notion is presented that endogenously produced anandamide (AEA) and 2-arachidonoylglycerol (2-AG) serve as autocrine or paracrine stimulators of the CB receptors, giving the appearance of constitutive activity. It is proposed that one cannot interpret inverse agonist studies without inference to the receptors' environment vis-à-vis the endocannabinoid agonists which themselves are highly lipophilic compounds with a preference for membranes. The endocannabinoid tone is governed by a combination of synthetic pathways and inactivation involving transport and degradation. The synthesis and degradation of 2-AG is well characterized, and 2-AG has been strongly implicated in retrograde signalling in neurons. Data implicating endocannabinoids in paracrine regulation have been described. Endocannabinoid ligands can traverse the cell's interior and potentially be stored on fatty acid-binding proteins (FABPs). Molecular modelling predicts that the endocannabinoids derived from membrane phospholipids can laterally diffuse to enter the CB receptor from the lipid bilayer. Considering that endocannabinoid signalling to CB receptors is a much more likely scenario than is receptor activation in the absence of agonist ligands, researchers are advised to refrain from assuming constitutive activity except for experimental models known to be devoid of endocannabinoid ligands. LINKED ARTICLESThis article is part of a themed issue on Cannabinoids in Biology and Medicine. To view the other articles in this issue visit http://dx.doi.org/10. 1111/bph.2011.163.issue-7 Abbreviations 2-AG, 2-arachidonoylglycerol; ABHD4,6 or 12, a/b hydrolase domain 4 (6 or 12); AEA, anandamide or N-arachidonylethanolamide; BRET, bioluminescence resonance energy transfer; CHO, Chinese hamster ovary cells; DAGL, diacylglycerol lipase; DSI or DSE, depolarization-induced suppression of inhibition or excitation; EPSP or IPSP, excitatory or inhibitory post-synaptic potential; ER, endoplasmic reticulum; FAAH, fatty acid amide hydrolase; FABP, fatty acid-binding protein; GPCR, G protein-coupled receptor; GP-NAE, glycerophospho-N-acylethanolamine; HEK293, human embryonic kidney cells clone 293; HFS, high-frequency stimulation; HSP, heat shock protein; IL3, intracellular loop 3; LPS, lipopolysaccharide; LTP, long-term potentiation; MAGL, monoacylglycerol lipase; MAPK, mitogen-activated protein kinase; NAE, N-acylethanolamine; NAPE, N-acyl phosphatidylethanolamine; NArPE, N-arachidonyl phosphatidylethanolamine NAT, N-acyl transferase; NMDA, N-methyl-D-aspartate; OEA, N-oleoylethanolamine; PEA, Npalmitoylethanolamine; PLC, phospholipase C; PLD, phospholipase D; POPC, palmitoyl, oleoyl-phosphatidylcholine; PTP, protein tyrosine phosphatase; TMH, transmembrane helix BJP British Journal of Pharmacology DOI:10.1111DOI:10. /j.1476DOI:10. -5381.2...

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“…Sokal et al (2008) found that the CB 1 receptor antagonist SR141716A blocked the potentiation of the fEPSP slope observed following HFS to the perforant path. However, other studies conducted on hippocampal slices of the Schaffer collateral–CA1 synapses have shown that CB 1 blockade favors LTP in the hippocampus (Slanina et al, 2005) and that mice lacking CB 1 receptors show enhanced LTP (Bohme et al, 2000).…”

Section: Cannabinoid Agonists Impair Hippocampal Synaptic Plasticitymentioning

confidence: 99%

The Role of Cannabinoids in Modulating Emotional and Non-Emotional Memory Processes in the Hippocampus

Akirav¹

2011

Front. Behav. Neurosci.

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Cannabinoid agonists generally have a disruptive effect on memory, learning, and operant behavior that is considered to be hippocampus-dependent. Nevertheless, under certain conditions, cannabinoid receptor activation may facilitate neuronal learning processes. For example, CB1 receptors are essential for the extinction of conditioned fear associations, indicating an important role for this receptor in neuronal emotional learning and memory. This review examines the diverse effects of cannabinoids on hippocampal memory and plasticity. It shows how the effects of cannabinoid receptor activation may vary depending on the route of administration, the nature of the task (aversive or not), and whether it involves emotional memory formation (e.g., conditioned fear and extinction learning) or non-emotional memory formation (e.g., spatial learning). It also examines the memory stage under investigation (acquisition, consolidation, retrieval, extinction), and the brain areas involved. Differences between the effects of exogenous and endogenous agonists are also discussed. The apparently biphasic effects of cannabinoids on anxiety is noted as this implies that the effects of cannabinoid receptor agonists on hippocampal learning and memory may be attributable to a general modulation of anxiety or stress levels and not to memory per se. The review concludes that cannabinoids have diverse effects on hippocampal memory and plasticity that cannot be categorized simply into an impairing or an enhancing effect. A better understanding of the involvement of cannabinoids in memory processes will help determine whether the benefits of the clinical use of cannabinoids outweigh the risks of possible memory impairments.

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The CB1 receptor antagonist, SR141716A, prevents high-frequency stimulation-induced reduction of feedback inhibition in the rat dentate gyrus following perforant path stimulation in vivo

Cited by 7 publications

References 29 publications

Cannabinoids modulate hippocampal memory and plasticity

Cannabinoids modulate hippocampal memory and plasticity

Endocannabinoid tone versus constitutive activity of cannabinoid receptors

The Role of Cannabinoids in Modulating Emotional and Non-Emotional Memory Processes in the Hippocampus

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