JohnBoy2000
Bluelighter
- Joined
- May 11, 2016
- Messages
- 2,473
I'm pretty sure Ki values are determined in vitro with a cloned receptor. It's an equilibrium constant that can be interpreted as affinity. I don't remember if its specifically for displacement of the ligand or just bound/not bound.
But PET scans are on living patients and are not at all sensitive enough for that
They would both use radiolabels, but Ki would be a scintillation deal--fancy Geiger counter.
It's why you can't rely on Ki for physiological results.
The PET scan would show which brain regions are affected based on metabolism of the ligand. I guess they can get a very rough idea about saturation.
That doesn't mean it's more potent--maybe bupropion does too if you eat the whole bottle. Potency is just dose/result. High potency main benefits are fewer side effect issues.
I also don't know that saturation is that desirable.
That atomoxetine study referred to saturation, but at clinically used doses.
The purpose I believe to imply that, at pharmacologically administered quantities, it can saturate the transporter.
Not desirable?
I assume you mean in relation the post synaptic receptor?
This saturation would be relative to the pre-synaptic transporter protein.
That wouldn't be desirable because?