Sandbox reserved 915: Difference between revisions
No edit summary |
No edit summary |
||
| Line 12: | Line 12: | ||
MGL also degrades [http://en.wikipedia.org/wiki/2-Arachidonoylglycerol 2-Arachidonoylglycerol] (2-AG), an [http://books.google.com/booksid=BxfLB4n3uoMC&pg=PA34&lpg=PA34&dq=hydrolysis+of+2-AG+by+MGL&source=bl&ots=R6Xm0KgGdK&sig=K3AwwtDNxbNUKJoa3zsd_25wVKs&hl=en&sa=X&ei=yOI5U43kCcbUsAT9_4DoBw&ved=0CGEQ6AEwCg#v=onepage&q=hydrolysis%20of%202-AG%20by%20MGL&f=false endocannabinoid], | MGL also degrades [http://en.wikipedia.org/wiki/2-Arachidonoylglycerol 2-Arachidonoylglycerol] (2-AG), an [http://books.google.com/booksid=BxfLB4n3uoMC&pg=PA34&lpg=PA34&dq=hydrolysis+of+2-AG+by+MGL&source=bl&ots=R6Xm0KgGdK&sig=K3AwwtDNxbNUKJoa3zsd_25wVKs&hl=en&sa=X&ei=yOI5U43kCcbUsAT9_4DoBw&ved=0CGEQ6AEwCg#v=onepage&q=hydrolysis%20of%202-AG%20by%20MGL&f=false endocannabinoid], | ||
to a glycerol and arachidonic acid. <ref name="Clemente"/> In the brain, endocannabinoids (ECs)are released from postsynaptic neurons, causing the retrograde suppression of synaptic transmission. <ref name="Taschler"/> | to a glycerol and arachidonic acid. <ref name="Clemente"/> In the brain, endocannabinoids (ECs)are released from postsynaptic neurons, causing the retrograde suppression of synaptic transmission. <ref name="Taschler"/> | ||
In peripheral tissues, endocannabinoids (ECs) are active in autonomic nervous system. EC signalling affects processes such as learning, motor control, cognition, and pain <ref name="Taschler" />. EC signalling is also able to regulate lipid metabolism and food intake. Looking at the role of MGL in energy metabolism, a deficiency in MGL in animals led to the buildup of 2-AG <ref name="Taschler" />. | In peripheral tissues, endocannabinoids (ECs) are active in autonomic nervous system. EC signalling affects processes such as learning, motor control, cognition, and pain <ref name="Taschler" />. EC signalling is also able to regulate lipid metabolism and food intake. Looking at the role of MGL in energy metabolism, a deficiency in MGL in animals led to the buildup of 2-AG <ref name="Taschler" />. The endocannabinoid 2-AG has a nociceptive effect in pain signalling <ref name="Clemente" />. MGL degrades 2-AG, preventing 2-AG from remaining bound to the cannabinoid receptor and therefore terminating the pain signal. Without the degradation of 2-AG by MGL, 2-AG levels would increase which would lead to a prolonged nociceptive effect <ref name="Clemente" /> | ||
===Inhibition of MGL=== | ===Inhibition of MGL=== | ||