In both systems, there is substantial storage of the transmitter in presynaptic membrane, enclosed vesicles. The vesicles fuse with the cell membrane when a depolarized stimulus comes down the pike and calcium is present, these membranes fuse and the goodie gets out into the synaptic arena by a process called exocytosis that works for many, in fact, most neurotransmitter and many endocrine systems that require an active molecule to get outside of the cell in which its made. That process, again, involves fusion of the vesicle and the cell membrane.
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The receptive cells in the environment contain a number of receptors that include notably the alpha receptors and the beta receptors. To make a long story short, facilitating transmission through alpha-1 and beta would be a good thing for mood elevation. But drugs that stimulate those receptors tend to have an up-effect on activity, mood, arousal and so on and it would be nice if we could jazz up those steps in neurotransmission by giving an antidepressant. But it’s more complicated than that and I will get back to that point in a minute.
This whole process is inactivated by actively pumping the amine back into the presynaptic nerve terminal by a process called transport that works by very specific large proteins sitting on the membrane that work in concert with the sodium pumping mechanism to energetically pull the amine back into the presynaptic cell where it can be recycled into vesicles and go around again or swept up by the janitor neuroterminal sitting in the membranes of the mitochondria of which there are many in the nerve terminal.
Obviously if you block MAO in the nerve terminal, you’ll make more serotonin, norepinephrine and even dopamine available and indirectly enhance their transmission. But the reuptake process is critically important physiologically and this process is selectively blocked by various antidepressant drugs. The tricyclics, especially the secondary amine tricyclics for the adrenergic system and the serotonin reuptake inhibitors for the serotonin system but they’re very similar in both systems.
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The other thing that happens at least with the tricyclic antidepressants is that they have variable affinity for adrenergic receptors and that leads to the more complete story of how these drugs work. It turns out that most antidepressant drugs and especially the tricyclics have very low affinity at beta receptors, very low affinity at alpha-2 receptors and it means that those two receptors lie naked to the increased availability of the transmitter when you block its inactivation by blocking the uptake process.
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What happens over several days to weeks is that alpha-2 and beta down-regulate, desensitize, get out of the way and stop working. Now that’s bad news for loss of the potentially useful mood elevating effect through beta but that’s part of the price of this business. It’s good news that you knock out the alpha-2 system because the alpha-2 receptors are autoreceptors. One of the first things that happens after you block the reuptake is that complicated feedback processes including local alpha-2 feedback shuts down the adrenergic system. So you get this paradoxical reaction of shutting down and then gradually over two or three weeks as the drug begins to work clinically these alpha_2 autoreceptors are knocked out of commission. So the presynaptic machinery revs up again.