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Endocannabinoid transmembrane

While the molecular identities of the proteins involved are not yet understood, it is clear that neurons and other cell types accumulate AEA intracellularly (Hillard and Jarrahian 2003). There are several characteristics of endocannabinoid transmembrane movement that are well supported by data obtained in multiple laboratories. To summarize, the accumulation of AEA by cells does not require sodium or ATP and is moderately temperature dependent. The accumulation exhibits saturation in the micromolar range and is inhibitable by a variety of structural analogs of AEA, suggesting that AEA accumulation involves its interaction with a saturable cellular component. Some data are consistent with the component being a plasma membrane transporter (see for example Hillard and Jarrahian 2000 Ronesi et al. 2004) while other data indicate that, in some cells, the accumulation is driven by... [Pg.198]

Keywords Adenylyl cyclase Aminoalkylindole Anandamide Ca Cannabinoid Cyclic AMP Depolarization suppression of inhibition or excitation Desensitization Endocannabinoid G proteins Ion channels Mitogen activated protein kinases Neurotransmission Nitric oxide Serine/threonine kinases Seven-transmembrane spanning receptors Synaptic plasticity Tyrosine kinases... [Pg.54]


See other pages where Endocannabinoid transmembrane is mentioned: [Pg.187]    [Pg.198]    [Pg.187]    [Pg.198]    [Pg.46]    [Pg.443]    [Pg.906]    [Pg.188]    [Pg.105]    [Pg.16]    [Pg.22]    [Pg.84]    [Pg.91]    [Pg.453]   


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