Barbiturates are Chloride Channel Openers, the only ones in existance!

[Kittycat5]

I don't really understand the difference. You are talking about cause (change in channel kinetics) and effect (change in the frequency of channel opening). If you look at single channel recordings, you can clearly see that the channel fluctuates between conductance and non-conductance states more often in the presence of benzodiazepines, hence why people say that the frequency of channel opening increases.

There really isnt a difference. They just keep the channel closed less often, which results in it being open more frequently. Same thing, different words.

 

[Anxious.Individual]

It is certainly true that barbiturates activate ligand-gated chloride channels. But barbiturates don't bind to all chloride channels. Voltage-gated chloride channels are not activated.

I didn't know, thanks for the info.

Nice info, source? Also serotonin, you said barbiturates activate v-gated cl- channels but then go on to say v-gated cl- channels aren't activated. What do you mean by this?

No specific source, this post is just some of the info that has built up in my head after many years of research on GABAergics.

Anxious.Individual

 

[Kdem]

Is there anything known about how this effects can be reversed - leading to the possibility for a treatment for GABAergic addiction (including ethanol)?

The point about flumazenil & adenosine which allows people to settle on a much lower dose of a BZD than previously is very intriguing.

Adenosine.

Are you suggesting that 'increasing' adenosine can be helpful for tapering benzodiazepines ?
In that case, meprobamate (a potent adenosine reuptake inhibitor) would work.

 

[Seppi]

I really doubt barbiturates open calcium-activated chloride channels like ANO1.