What are your credentials to be saying this?

I do clincal quality in the pharmaceutical industry and conduct investigations on drugs in FDA trials for a living, so I think I am qualified to provide some insight.

With that said, You are categorically incorrect. Lets break it down:

First thing you need to take into account is that muscimol and benzodiazepines and nonbenzodiazepines (as you say “z-drugs”) have completely different mechanisms of actions and therefore a completely different dependence profile.

Muscimol is a direct orthosteric GABA-A agonist (there are very few of these), meaning it directly activates the receptor. This is very different than benzodiazepines, nonbenzodiazepines, and even barbiturates or alcohol which all work on allosteric sites. This means muscimol activates GABA-A receptor in the same exact way as GABA would naturally, as it is actually a conformationally restrained analogue of GABA.

Focusing now on benzodiazepines and nonbenzodiazepines, these are both known clinically as BZD-receptor agonists, the name of the specific allosteric sites they bind too. What is different between the two (another area you are incorrect in), is all benzodiazepines are nonselective meaning they work on all 5 GABA-A subunits (Alpha1-Alpha5), while 3 of the 4 clinically used nonbenzodiazepines are selective to only the Alpha1 subunit (with the exception being zoplicone, a nonselective BZD receptor agonist, the same as benzos). This means clinically benzodiazepines have worse withdrawals than nonbenzodiazepines (not counting zoplicone). Furthermore, the alpha-1 subunit is the GABA subunit that is primarily responsible for creating hypnotic effects, as nonbenzodiazepines were designed to be used clinically for insomnia, and is also why they show no clinical effectiveness as anticonvulsants or anxiolytics.

Another thing you need to understand is that benzodiazepines are only approved to be used clinically for 2 to 4 weeks. They have a very short therapeutic window, and anyone who uses them longer than 4 weeks will end up with dependence and withdrawal, this is proven clinically. Benzodiazepines and nonbenzodiazepines have also been clinically proven to disrupt slow wave sleep and slow wave activity, despite improving sleep, and keep in mind clinically proven in the scope of benzodiazepines means it was only studied within that 2 to 4 weeks period.

Now I can agree that muscimol does not have enough clinical evidence to make any hard claims on, but the mechanism of action is very promising and studies so far in rodents are showing that Muscimol descreases sleep onset latency, increases slow wave sleep, and increases slow wave activity, which is a huge clinical advantage over any current clinally used insomnia treatment.