Compounds > 3-(2-hydroxy-4-(1-1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol

3-(2-hydroxy-4-(1-1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol and thiazolyl-blue

3-(2-hydroxy-4-(1-1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol has been researched along with thiazolyl-blue* in 1 studies

Other Studies

1 other study(ies) available for 3-(2-hydroxy-4-(1-1-dimethylheptyl)phenyl)-4-(3-hydroxypropyl)cyclohexanol and thiazolyl-blue

Article	Year
Depolarization and Ca(2+) down regulate CB1 receptors and CB1-mediated signaling in cerebellar granule neurons. Neuropharmacology, 2006, Volume: 50, Issue:6 Presynaptic terminals of cerebellar granule neurons are primary targets of cannabinoids, which act through type 1 G alpha(i/o)-coupled cannabinoid receptors (CB1) to modulate glutamate release. To study CB1 signaling investigators use primary cultures of granule neurons, typically grown in medium supplemented with elevated KCl to improve long-term survival. Herein, we demonstrate that CB1 expression and signaling are perturbed under these conditions. Specifically, immunochemical and RT-PCR assays indicate that depolarizing growth conditions decrease CB1 protein, mRNA and CB1-mediated inhibition of adenylyl cyclase compared to cultures grown in physiologic medium containing 5mM KCl. Depolarization-dependent downregulation of CB1 mRNA, like survival, is attenuated by L-type VDCC antagonists but not the Na(+)-channel antagonist, tetrodotoxin. Comparison of oligonucleotide microarrays from cultures grown in 5mM versus 25 mM KCl confirms that depolarization reduces CB1 mRNA, but not mRNAs encoding several G-protein subunits or adenylyl cyclases. However, significant alterations in synaptic signaling proteins that likely lie downstream of CB1 are observed, including K(+) channels, alpha-neurexins, cAMP-GEFII, Munc13-3, secretogranin and synaptotagmin. These findings make a compelling argument to adopt cultures grown in 5mM KCl for future study of CB1 signaling in granule neurons. Further, they suggest that a depolarization and Ca(2+)-dependent signaling pathway represses CB1 gene transcription. Topics: Age Factors; Analysis of Variance; Animals; Animals, Newborn; Blotting, Northern; Calcium; Calcium Channel Blockers; Cell Survival; Cells, Cultured; Cerebellum; Cyclohexanols; Dose-Response Relationship, Drug; Drug Interactions; Fluorescent Antibody Technique; Gene Expression Regulation, Developmental; In Situ Hybridization; Models, Biological; Neurons; Nifedipine; Potassium Chloride; Rats; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB1; Signal Transduction; Tetrazolium Salts; Tetrodotoxin; Thiazoles; Time Factors	2006

Article

Year

Depolarization and Ca(2+) down regulate CB1 receptors and CB1-mediated signaling in cerebellar granule neurons.

Neuropharmacology, 2006, Volume: 50, Issue:6

Presynaptic terminals of cerebellar granule neurons are primary targets of cannabinoids, which act through type 1 G alpha(i/o)-coupled cannabinoid receptors (CB1) to modulate glutamate release. To study CB1 signaling investigators use primary cultures of granule neurons, typically grown in medium supplemented with elevated KCl to improve long-term survival. Herein, we demonstrate that CB1 expression and signaling are perturbed under these conditions. Specifically, immunochemical and RT-PCR assays indicate that depolarizing growth conditions decrease CB1 protein, mRNA and CB1-mediated inhibition of adenylyl cyclase compared to cultures grown in physiologic medium containing 5mM KCl. Depolarization-dependent downregulation of CB1 mRNA, like survival, is attenuated by L-type VDCC antagonists but not the Na(+)-channel antagonist, tetrodotoxin. Comparison of oligonucleotide microarrays from cultures grown in 5mM versus 25 mM KCl confirms that depolarization reduces CB1 mRNA, but not mRNAs encoding several G-protein subunits or adenylyl cyclases. However, significant alterations in synaptic signaling proteins that likely lie downstream of CB1 are observed, including K(+) channels, alpha-neurexins, cAMP-GEFII, Munc13-3, secretogranin and synaptotagmin. These findings make a compelling argument to adopt cultures grown in 5mM KCl for future study of CB1 signaling in granule neurons. Further, they suggest that a depolarization and Ca(2+)-dependent signaling pathway represses CB1 gene transcription.

Topics: Age Factors; Analysis of Variance; Animals; Animals, Newborn; Blotting, Northern; Calcium; Calcium Channel Blockers; Cell Survival; Cells, Cultured; Cerebellum; Cyclohexanols; Dose-Response Relationship, Drug; Drug Interactions; Fluorescent Antibody Technique; Gene Expression Regulation, Developmental; In Situ Hybridization; Models, Biological; Neurons; Nifedipine; Potassium Chloride; Rats; Rats, Sprague-Dawley; Receptor, Cannabinoid, CB1; Signal Transduction; Tetrazolium Salts; Tetrodotoxin; Thiazoles; Time Factors

2006