thapsigargin/cannabis

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Identification of N-arachidonoyl dopamine as a highly biased ligand at cannabinoid CB1 receptors.

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OBJECTIVE N-arachidonyl dopamine (NADA) has been identified as a putative endocannabinoid, but there is little information about which signalling pathways it activates. The purpose of this study was to identify the signalling pathways activated by NADA in vitro. METHODS Human or rat cannabinoid CB1

Signaling pathways from cannabinoid receptor-1 activation to inhibition of N-methyl-D-aspartic acid mediated calcium influx and neurotoxicity in dorsal root ganglion neurons.

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Although the activation of cannabinoid receptor-1 (CB1) receptors by cannabinoids is known to inhibit neuronal hyperexcitability and reduce excitotoxic cell death, the mechanistic links between these two actions remain elusive. We tested the hypothesis that activation of CB1 receptors inhibits

Signal transduction of cannabinoid CB1 receptors in a smooth muscle cell line.

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1. The effects of cannabinoid (CB) receptor stimulation on membrane currents in single cells from the Syrian hamster vas deferens cell line DDT1MF-2 were investigated using the whole cell patch clamp technique. 2. The CB receptor agonist CP55,940 evoked a concentration-dependent transient outward

Characterization of human cannabinoid CB2 receptor coupled to chimeric Galpha(qi5) and Galpha(qo5) proteins.

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Cannabinoid CB(2) receptors may couple to a variety of G proteins and intracellular effector systems to regulate physiological and pathophysiological processes involved in inflammatory and neuropathic pain. In this study, the coupling of cannabinoid hCB(2) receptors to Galpha(qo5) and Galpha(qi5)

Novel effect of CP55,940, a CB1/CB2 cannabinoid receptor agonist, on intracellular free Ca2+ levels in bladder cancer cells.

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The study was undertaken to explore the effect of CP55,940 ((-)-cis-3-[2-Hydroxy4-(1,1-dimethylheptyl) phenyl]-trans-4-(3-hydroxypropyl)cyclohexanol), a drug commonly used as a CB1/CB2 cannabinoid receptor agonist, on intracellular free Ca2+ levels ([Ca2+]i) in several cell types [Ca2+]i was

Arachidonic acid mediates non-capacitative calcium entry evoked by CB1-cannabinoid receptor activation in DDT1 MF-2 smooth muscle cells.

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Cannabinoid CB1-receptor stimulation in DDT1 MF-2 smooth muscle cells induces a rise in [Ca2+]i, which is dependent on extracellular Ca2+ and modulated by thapsigargin-sensitive stores, suggesting capacitative Ca2+ entry (CCE), and by MAP kinase. Non-capacitative Ca2+ entry (NCCE) stimulated by

Modulation of cannabinoid-induced antinociception after intracerebroventricular versus intrathecal administration to mice: possible mechanisms for interaction with morphine.

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Dose-effect curves were generated for the cannabinoids [intracerebroventricularly (icv.)] and compared with those previously generated after administration intrathecally (i.t.). The ED50 values after administration of levonantradol, CP 55,940, delta 9-THC and delta 8-THC i.t. vs. icv. did not differ

Signaling Mechanism of Cannabinoid Receptor-2 Activation-Induced β-Endorphin Release.

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Activation of cannabinoid receptor-2 (CB2) results in β-endorphin release from keratinocytes, which then acts on primary afferent neurons to inhibit nociception. However, the underlying mechanism is still unknown. The CB2 receptor is generally thought to couple to Gi/o to inhibit cAMP production,

Ryanodine receptor regulates endogenous cannabinoid mobilization in the hippocampus.

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Endogenous cannabinoids (eCBs) are produced and mobilized in a cytosolic calcium ([Ca2+]i)-dependent manner, and they regulate excitatory and inhibitory neurotransmitter release by acting as retrograde messengers. An indirect but real-time bioassay for this process on GABAergic transmission is DSI

The cannabinoid agonist WIN55,212-2 increases intracellular calcium via CB1 receptor coupling to Gq/11 G proteins.

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Central nervous system responses to cannabis are primarily mediated by CB(1) receptors, which couple preferentially to G(i/o) G proteins. Here, we used calcium photometry to monitor the effect of CB(1) activation on intracellular calcium concentration. Perfusion with 5 microM CB(1) aminoalkylindole

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