4 replies to this topic

[Reformed-Redan]

I'm looking at this compound now and am convinced it would normalize glutamate hypofunction and dopamine hypo/hyper(function) in the brain('s) of schizophrenics. I would sure as hell want to try GTS-21; but, from what I've gathered it is too difficult to synthesize. Thoughts?

 

Check, http://en.wikipedia....iki/PNU-120,596

 

Interesting compound, and better yet, it's a PAM so no issues with tolerance or receptor downregulation. I'm thinking in combination with something like piracetam that upregulates NMDA receptors, it could wipe away both positive and negative symptoms of schizophrenia and possibly the negative aspects of depression. Thoughts? 

[goodman]

if its too good to be true it prbly isnt

[focus83]

Why wouldn't be there no issues with receptor downregulation and tolerance? Benzodiazepines are also allosteric modulators and downregulation as well as tolerance are major issues. Can you elaborate?

[Reformed-Redan]

Why wouldn't be there no issues with receptor downregulation and tolerance? Benzodiazepines are also allosteric modulators and downregulation as well as tolerance are major issues. Can you elaborate?

Positive allosteric modulators tend to not cause downregulation via autorecepter feedback during receptor occupancy by an agonist. Partial agonists tend to sidestep that issue, yet with time compensatory mechanisms

 

(homeostasis) seems to take hold of the action and balance out whatever inequality there may have been. They seem to be less prone to down-regulating receptors via feedback mechanisms (positive allosteric modulators that

 

is), of which I only have a superficial understanding of. Basically, I think, they change the voltage channels and frequency of firing, through gating mechanisms, without interfering with the amount of whatever aforementioned

 

transmitter. So, positive allosteric modulators, will increase the frequency of synapses firing, while negative allosteric modualtors will decrease the frequency of spontaneous firing of neurons through whatever mechanism takes

 

place in the synaptic cleft or even outside of it (think, glia cells.)

[lourdaud]

Why wouldn't be there no issues with receptor downregulation and tolerance? Benzodiazepines are also allosteric modulators and downregulation as well as tolerance are major issues. Can you elaborate?

 

+1

There's already galantamine (also a PAM at a7n) and it works very well, unfortunately tolerance builds up just after a few days..