By Attila Köfalvi
Endocannabinoids have large healing capability. This ebook introduces readers to our present realizing of the neurobiology of endocannabinoids and similar structures, detailing their pathophysiological position and healing strength. Authors, skilled scientific investigators, current and research result of contemporary scientific trials in addition to the advance of latest healing options and medicines.
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Extra info for Cannabinoids and the brain
J Neurochem 84:585–591. Basavarajappa BS, Hungund BL (1999) Chronic ethanol increases the cannabinoid receptor agonist anandamide and its precursor N-arachidonoylphosphatidylethanolamine in SK-N-SH cells. J Neurochem 72:522–528. Basavarajappa BS, Saito M, Cooper TB, Hungund BL (2000) Stimulation of cannabinoid receptor agonist 2-arachidonylglycerol by chronic ethanol and its modulation by specific neuromodulators in cerebellar granule neurons. Biochim Biophys Acta 1535:78–86. Beaulieu P, Bisogno T, Punwar S, Farquhar-Smith WP, Ambrosino G, Di Marzo V, Rice AS (2000) Role of the endogenous cannabinoid system in the formalin test of persistent pain in the rat.
The following citation can be instructive in this respect: “Translocation… across the plasma membrane is achieved by a concert of co-existing mechanisms. , 2006). The citation in question refers to the cellular uptake of long chain fatty acids, which have been the subject of investigation long before the discovery of AEA, but which have grappled with the same sort of issues as those for AEA uptake. In the absence of a published report concerning the identification and cloning of an AEA transporter Table 1 The case for/against a facilitated transport mechanism of AEA uptake Evidence in favour of facilitated transport Alternative explanations/observations AEA is concentrated in cells to a greater extent than would be predicted on the basis of a passive diffusion processa The extracellular–intracellular gradient is partly driven in some (but not all) cells by FAAH-catalysed metabolism of AEAi,j; intracellular sequestration of AEAa would also act to keep the free [AEA]i low and allow for further passive diffusion Initial rapid uptake is not saturable, and its temperature dependency reflects effects upon AEA availability rather than the uptake process itselfj,k N-Acylethanolamines form complexes with cholesteroll which is present in plasma membranes at much greater concentrations than in intracellular membranesd Uptake is time and temperature dependent and shows saturability, but is not coupled to any ion gradient or dependent upon ATPb,c Vesicles prepared from plasma membranes accumulate AEA whereas vesicles prepared from intracellular membranes do not; the FAAH activity of the cells is associated with the latter rather than the former; Cholesterol depletion of some (but not all) cells reduces uptaked,e Uptake can be inhibited pharmacologically, even in cells lacking FAAHf,g; the inhibitors have pharmacological effects in vivoh FAAH is inhibited by the compounds, and in the absence of this enzyme, the in vitro potencies of the uptake inhibitors are modest (see Fig.
Biochem J 316:977–984. Di Marzo V, De Petrocellis L, Sugiura T, Waku K (1996b) Potential biosynthetic connections between the two cannabimimetic eicosanoids, anandamide and 2-arachidonoyl-glycerol, in mouse neuroblastoma cells. Biochem Biophys Res Commun 227:281–288. Di Marzo V, Bisogno T, De Petrocellis L, Melck D, Orlando P, Wagner JA, Kunos G (1999) Biosynthesis and inactivation of the endocannabinoid 2-arachidonoylglycerol in circulating and tumoral macrophages. Eur J Biochem 264:258–267. Di Marzo V, De Petrocellis L, Bisogno T, Berger A, Mechoulam R (2002) Biology of endocannabinoids.