LEADER 06361nam 22008895 450 001 9910298267903321 005 20220727194510.0 010 $a3-319-20825-X 024 7 $a10.1007/978-3-319-20825-1 035 $a(CKB)3710000000479184 035 $a(EBL)4178347 035 $a(SSID)ssj0001583189 035 $a(PQKBManifestationID)16258188 035 $a(PQKBTitleCode)TC0001583189 035 $a(PQKBWorkID)14861988 035 $a(PQKB)10842333 035 $a(DE-He213)978-3-319-20825-1 035 $a(MiAaPQ)EBC4178347 035 $a(PPN)190532556 035 $a(EXLCZ)993710000000479184 100 $a20150925d2015 u| 0 101 0 $aeng 135 $aur|n#---||||| 181 $ctxt 182 $cc 183 $acr 200 10$aEndocannabinoids /$fedited by Roger G. Pertwee 205 $a1st ed. 2015. 210 1$aCham :$cSpringer International Publishing :$cImprint: Springer,$d2015. 215 $a1 online resource (477 p.) 225 1 $aHandbook of Experimental Pharmacology,$x0171-2004 ;$v231 300 $aDescription based upon print version of record. 311 18$a3-319-20824-1 320 $aIncludes bibliographical references at the end of each chapters and index. 327 $aPreface; The Endocannabinoid System: A Look Back and Ahead; Contents; Endocannabinoids and Their Pharmacological Actions; 1 Introduction; 2 Evidence That Certain Endogenous Compounds Target Cannabinoid Receptors Orthosterically; 2.1 Evidence from Binding Assays; 2.2 Evidence from Two Functional Bioassays; 2.2.1 [35S]GTPgammaS Binding Assay; 2.2.2 Cyclic AMP Assay; 3 Non-Cannabinoid Receptors and Channels Targeted by Endogenous Cannabinoid Receptor Ligands at Submicromolar Concentrations; 3.1 Non-Cannabinoid G Protein-Coupled Receptors; 3.1.1 GPR55; 3.2 Ligand-Gated Ion Channels 327 $a3.2.1 5-HT3 Receptors3.2.2 Nicotinic Acetylcholine Receptors; 3.2.3 Glycine Receptors; 3.2.4 Ionotropic Glutamate NMDA Receptors; 3.3 Transient Receptor Potential Channels; 3.3.1 TRPV1; 3.3.2 TRPM8 Channels; 3.4 Voltage-Gated Calcium Channels; 3.4.1 T-Type Cav3 Calcium Channels; 3.5 Potassium Channels; 3.5.1 ATP-Sensitive Inward Rectifier KATP Channels of the 2TM Domain Family; 3.5.2 Voltage-Gated Kv and KCa Channels of the 6TM Domain Family; 4 Allosteric Endocannabinoids; 5 Conclusions; References; Biosynthesis and Fate of Endocannabinoids 327 $a1 Endocannabinoids and Endocannabinoid-Like Compounds2 Biosynthesis of the Endocannabinoids; 3 Uptake of the Endocannabinoids: Proposed Mechanisms; 4 Degradation of the Endocannabinoids; 4.1 FAAH and NAAA; 4.2 MGL, ABHD6 and ABHD12; 5 Conclusions; References; Distribution of the Endocannabinoid System in the Central Nervous System; 1 Introduction; 1.1 Overview; 1.2 Cells Expressing Components of the ECS; 1.3 Subcellular Localization of CB1 Cannabinoid Receptors; 2 Retina; 2.1 Receptors; 2.2 Synthetic Enzymes; 2.3 Degradative Enzymes; 3 Cerebral Cortex; 3.1 Neocortex; 3.1.1 Receptors 327 $a3.1.2 Synthetic Enzymes3.1.3 Degradative Enzymes; 3.2 Olfactory Areas (Olfactory Bulb, Piriform Cortex, Associated Regions); 3.2.1 Receptors; 3.2.2 Synthetic Enzymes; 3.2.3 Degradative Enzymes; 3.3 Hippocampal Formation; 3.3.1 Receptors; 3.3.2 Synthetic Enzymes; 3.3.3 Degradative Enzymes; 3.4 Cortical Subplate (Other Amygdala Nuclei); 3.4.1 Receptors; 3.4.2 Synthetic Enzymes; 3.4.3 Degradative Enzymes; 4 Subcortical Nuclei (Striatum, Basal Ganglia); 4.1 Striatum (Dorsal, Caudate); 4.1.1 Receptors; 4.1.2 Synthetic Enzymes; 4.1.3 Degradative Enzymes; 4.2 Striatum (Ventral, Accumbens) 327 $a4.2.1 Receptors4.2.2 Synthetic Enzymes; 4.2.3 Degradative Enzymes; 4.3 Striatum Medial (Lateral Septum, Septohippocampal, etc.); 4.3.1 Receptors; 4.3.2 Synthetic Enzymes; 4.3.3 Degradative Enzymes; 4.4 Striatum Caudal (Striatum-like Amygdala Nuclei, Central Amygdala, Bed Nucleus, Medial Amygdala, Etc.); 4.4.1 Receptors; 5 Cerebellum and Associated Nuclei; 5.1 Cerebellar Cortex; 5.1.1 Receptors; 5.1.2 Synthetic Enzymes; 5.1.3 Degradative Enzymes; 5.2 Deep Cerebellar Nuclei (Fastigial, Interpos, Dentate Nucleus); 5.2.1 Receptors; 5.2.2 Synthetic Enzymes; 5.2.3 Degradative Enzymes; 6 Brainstem 327 $a6.1 Diencephalon 330 $aThere is currently considerable interest in the development of medicines that would enhance endocannabinoid-induced ?autoprotection?, for example through inhibition of endocannabinoid metabolizing enzymes or cellular uptake processes or that would oppose endocannabinoid-induced ?autoimpairment?. 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