How exactly does the relationship between presynaptic alpha 2 adrenergic receptors and postsynaptic alpha 2 adrenergic receptors work?
I know that in abstract presynaptically NE binds to inhibit its own release and postsynaptically binds to produce stimulating effects, but what exactly changes in the postsynaptic binding sites due to activation of presynaptic binding sites? Is it like a closed channel where NE reaches presynaptic receptors, gets inhibited and the rest remaining binds to the postsynaptic receptors to produce stimulation?
I still struggle to find how alpha 2 agonists which are used to lower blood pressure by inhibiting NE somehow improve PFC function in ADHD people. Is their mechanism similar to reuptake inhibitors where there's more NE available for dopamine metabolism since the a2 agonist is taking up the a2 binding sites resulting in more NE and dopamine in other areas of the PFC?
I also find it fascinating how altered a2 receptor sensitivity plays a part in nearly every one of the main common mental illnesses and even orthostatic intolerance as well.
I know that in abstract presynaptically NE binds to inhibit its own release and postsynaptically binds to produce stimulating effects, but what exactly changes in the postsynaptic binding sites due to activation of presynaptic binding sites? Is it like a closed channel where NE reaches presynaptic receptors, gets inhibited and the rest remaining binds to the postsynaptic receptors to produce stimulation?
I still struggle to find how alpha 2 agonists which are used to lower blood pressure by inhibiting NE somehow improve PFC function in ADHD people. Is their mechanism similar to reuptake inhibitors where there's more NE available for dopamine metabolism since the a2 agonist is taking up the a2 binding sites resulting in more NE and dopamine in other areas of the PFC?
I also find it fascinating how altered a2 receptor sensitivity plays a part in nearly every one of the main common mental illnesses and even orthostatic intolerance as well.
