Posted by undopaminergic on October 17, 2021, at 8:21:02
In reply to Re: Ritalin + an MAOi = Greater baseline D/NE? » undopaminergic, posted by linkadge on October 15, 2021, at 21:07:00
> These are mice with double or triple gene knockouts.
OK, the problem with that approach is that these mice grow up to have a different neurobiology. The differences develop to compensate for the missing genes. Compensatory changes can be very far-reaching. I read about animals (rats or mice) that lacked a central (CNS) serotonergic system, and they survived!
> The problem is that the reuptake process is also needed for the recycling of the neurotransmitter.
>Yes, but this does not appear to seriously deplete the stores of the neurotransmitter, at least not the way reserpine or amphetamine can do.
> So blocking reuptake does cause activation of the inhibitory autoreceptors slowing firing, but also blocking the resorption of the neurotransmitter for subsequent re-release.
>
> Many reuptake inhibitors do more to 'stabilize' monoamine activity than really enhance it. The exception is the stimulants with a more complex mode of action.
>Well, the reuptake inhibitors can increase synaptic monoamine content with over 100%. That would surely boost the neurotransmission. Perhaps you mean that reuptake inhibitors only enhance existing, endogenous signals, and does not itself induce the neurons to fire, although they can boost weak signals that would not otherwise go through.
-undopaminergic
poster:undopaminergic
thread:1117157
URL: http://www.dr-bob.org/babble/20210723/msgs/1117277.html