Posted by linkadge on October 16, 2017, at 16:00:40
In reply to Re: NE strengths of Reboxetine vs Atomoxetine » linkadge, posted by MightyKondrian on October 14, 2017, at 15:26:45
I am not an expert either, but there are post-synaptic receptors (the ones that exert the main effect of the neurotransmitter) and there are pre-synaptic autoreceptors and heteroreceptors which affect the release of the neurotransmitter.
So, for example, if you take a reuptake inhibitor, you immediately increase the amount of neurotransmitter in the synapse. However, this activates the post-synaptic receptors and the autoreceptors. When the autoreceptors are activated, this slows the firing / release of the neurotransmitter from the presynaptic neuron.
Over time, the autoreceptors can desensitize which can result in increased firing.
Take, for example clonidine. It is a blood pressure medication which slows the release of norepinephrine. It does this by activating a specific norepinephrine autoreceptor (alpha-2). This receptor can also be activated by norepinephrine itself to slow the release of more neurotransmitter.
Mirtazapine and yohimbine block this same adrenaline receptor, which increases the firing of norepinephrine.
Basically, the autoreceptors work to control the amount of neurotransmitter in the synapse. They respond when the amount of neurotransmitter becomes elevated to slow the amount released.
Serotonin and dopamine also have autoreceptors which respond to serotonin and dopamine by releasing less neurotransmitter.
Linkadge
poster:linkadge
thread:1095398
URL: http://www.dr-bob.org/babble/20161215/msgs/1095460.html