And inhibitory neurons where they inhibit

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and inhibitory neurons where they inhibit neurotransmitter release Endocannabinoids are highly lipophilic and are derived from lipids in the plasma membrane. 2 major endogenous endocannabinoids: 2-arachidonylglycerol (2-AG) and anandamide (released in response to neuronal activity and activate CB1 receptors
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Endogenous endocannabinoids Both 2-AG and anandamide are synthesized from lipid precursors derived from the plasma membrane and release is coupled to synthesis (influx of Ca2+ actives synthetic enzymes) Synthesis can also be stimulated by activation of G-protein coupled receptors, specifically mGluRs and muscarinic receptors (i.e., Gq-coupled receptors which stimulate DAG production)
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Both 2-AG and anandamide function as retrograde messengers (are released from postsynaptic membrane and bind to CB1 receptors located presynaptically) inhibit presynpatic activity (actions can last from seconds to hours)
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CB1 activation also inhibits cAMP production. More longterm (and complicated) effects on gene expression and synaptic plasticity
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Endocannabinoid signaling is terminated by their transport into cells and hydrolysis ( fatty acid amide hydrolase or FAAH breaks down anandamide and monoacylglycerol lipase or MGL breaks down 2-AG) Endocannabinoids can diffuse passively through membranes, but transport is facilitated by endocannabinoid transporters . This is an energy independent transporter, it just facilitates passive diffusion.
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The role of endocannabinoid signaling in the hippocampus Action potentials in hippocampal pyramidal neurons cause synthesis of 2-AG 2-AG diffuses out and activates CB1 receptors on GABA inter-neurons Reduction in GABA signaling, less inhibition of the pyramidal neuron May play a role in long term potentiation, but what happens when you flood your CB1 receptors with THC?
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