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10.1016/j.celrep.2015.08.041 http://scihub22266oqcxt.onion/10.1016/j.celrep.2015.08.041 C4857883!4857883!26365195     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2015 ; 12 (12): 1997-2008 Nephropedia Template TP {{tp|p=26365195|t=2015. Cocaine-Induced Endocannabinoid Mobilization in the Ventral Tegmental Area |pdf=|usr=}}{{26365195}} gab.com Text Cocaine-Induced Endocannabinoid Mobilization in the Ventral Tegmental Area JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26365195 #FOAvip Cocaine is a highly addictive drug that acts upon the brain?s reward circuitry via the inhibition of mono-amine uptake. Endogenous cannabinoids (eCB) are lipid molecules released from midbrain dopamine (DA) neurons that modulate cocaine?s effects through poorly understood mechanisms. We find that cocaine stimulates release of the eCB, 2-arach-idonoylglycerol (2-AG), in the rat ventral midbrain to suppress GABAergic inhibition of DA neurons, through activation of presynaptic cannabinoid CB1 receptors. Cocaine mobilizes 2-AG via inhibition of norepinephrine uptake and promotion of a cooperative interaction between Gq/11-coupled type-1 metabotropic glutamate and ?1-adrenergic receptors to stimulate internal calcium stores and activate phospholipase C. The disinhibition of DA neurons by cocaine-mobilized 2-AG is also functionally relevant because it augments DA release in the nucleus accumbens in vivo. Our results identify a mechanism through which the eCB system can regulate the rewarding and addictive properties of cocaine. Twit Text FOAVip Cocaine-Induced Endocannabinoid Mobilization in the Ventral Tegmental Area ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=26365195 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26365195 #FOAvip English Wikipedia <ref>{{Cite pmid|26365195}}</ref> Cocaine-Induced Endocannabinoid Mobilization in the Ventral Tegmental Area #MMPMID26365195 Wang H; Treadway T; Covey DP; Cheer JF; Lupica CR Cell Rep 2015[Sep]; 12 (12): 1997-2008 PMID26365195show ga Cocaine is a highly addictive drug that acts upon the brain?s reward circuitry via the inhibition of mono-amine uptake. Endogenous cannabinoids (eCB) are lipid molecules released from midbrain dopamine (DA) neurons that modulate cocaine?s effects through poorly understood mechanisms. We find that cocaine stimulates release of the eCB, 2-arach-idonoylglycerol (2-AG), in the rat ventral midbrain to suppress GABAergic inhibition of DA neurons, through activation of presynaptic cannabinoid CB1 receptors. Cocaine mobilizes 2-AG via inhibition of norepinephrine uptake and promotion of a cooperative interaction between Gq/11-coupled type-1 metabotropic glutamate and ?1-adrenergic receptors to stimulate internal calcium stores and activate phospholipase C. The disinhibition of DA neurons by cocaine-mobilized 2-AG is also functionally relevant because it augments DA release in the nucleus accumbens in vivo. Our results identify a mechanism through which the eCB system can regulate the rewarding and addictive properties of cocaine. äCocaine-Induced Endocannabinoid Mobilization in the Ventral Tegmental (epmc).pdf DeepDyve Pubget Overpricing