Could GABA-A subunit cycling reduce tolerance?

I’ve been thinking about a theoretical way to reduce tolerance to GABA-A positive modulators by rotating subtype targeting instead of repeatedly hitting the same receptor population.

The core logic is:

• tolerance appears subunit-specific rather than uniform,

• receptor recovery may happen on a meaningful timescale,

• intermittent exposure seems to reduce tolerance compared with continuous exposure,

• selective ligands already exist for some subtypes.

The biggest weak point I can see is whether receptor recovery is actually fast and clean enough for cycling to work. If that assumption is wrong, the whole model may fall apart there.

I’m not claiming this is solved — I’m asking whether the model is biologically coherent, whether existing work already addresses it, and what the most likely failure point would be.

If this is nonsense, I’d rather know now. If it’s plausible, I’d like to refine it into something that could actually be studied.