Behavioral suppression induced by cannabinoids is due to activation of the arachidonic acid cascade in rats

@article{Yamaguchi2001BehavioralSI,
  title={Behavioral suppression induced by cannabinoids is due to activation of the arachidonic acid cascade in rats},
  author={Taku Yamaguchi and Yukihiro Shoyama and Shigenori Watanabe and Tsuneyuki Yamamoto},
  journal={Brain Research},
  year={2001},
  volume={889},
  pages={149-154}
}
Activation of brain prostanoid EP3 receptors via arachidonic acid cascade during behavioral suppression induced by Δ8‐tetrahydrocannabinol
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It is concluded that the suppression of lever‐pressing behavior by cannabinoid is due to activation of the prostanoid EP3 receptor through an elevation of PGE2 in the brain.
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Endocannabinoid System Modulates Relapse to Methamphetamine Seeking: Possible Mediation by the Arachidonic Acid Cascade
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The results suggest that endocannabinoid-activating substances as well as cyclooxygenase inhibitors may be promising as antirelapse agents and extend the current view on the treatment of drug dependence.
Indomethacin Enhances Type 1 Cannabinoid Receptor Signaling
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References

SHOWING 1-10 OF 31 REFERENCES
Molecular characterization of a peripheral receptor for cannabinoids
TLDR
The cloning of a receptor for cannabinoids is reported that is not expressed in the brain but rather in macrophages in the marginal zone of spleen, which helps clarify the non-psychoactive effects of cannabinoids.
Delta 9-tetrahydrocannabinol increases arachidonic acid levels in guinea pig cerebral cortex slices.
TLDR
In brain, as in extra-neural cells in culture, cannabinoids increase unesterified AA levels; however, the relative potencies of the cannabinoids the authors examined in increasing AA levels do not correlate well with their in vivo psychoactive potencies.
Structure of a cannabinoid receptor and functional expression of the cloned cDNA
TLDR
The cloning and expression of a complementary DNA that encodes a G protein-coupled receptor that is involved in cannabinoid-induced CNS effects (including alterations in mood and cognition) experienced by users of marijuana are suggested.
2-Arachidonoylglycerol: a possible endogenous cannabinoid receptor ligand in brain.
TLDR
2-Arachidonoylglycerol was shown to bind appreciably to the cannabinoid receptor in competitive inhibition experiments and may be an endogenous cannabinoid receptor ligand in the brain.
Nonclassical cannabinoid analgetics inhibit adenylate cyclase: development of a cannabinoid receptor model.
TLDR
It is postulated that the receptor that is associated with the regulation of adenylate cyclase in vitro may be the same receptor as that mediating analgesia in vivo, and a conceptualization of the cannabinoid analgetic receptor is presented.
Anandamide and delta 9-THC dilation of cerebral arterioles is blocked by indomethacin.
TLDR
Results show that AN and delta 9-THC can modulate cerebral arterioles, likely by stimulating release and metabolism of endogenous arachidonic acid, and whether dilation is due to vasodilator eicosanoids, or other vasoactive agents whose synthesis or release is cyclooxygenase dependent, is uncertain.
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