Ketamine and depression

[mippo]

Would someone so kindly point me the way to the most recent research being done using Ketamine to (darn near) cure depression?

Is this study still ongoing or possibly has it been published yet?

Thanks!

 

[23536]

http://clinicaltrials.gov/ct2/results?term=ketamine+depression

 

[Darksidesam]

only problem with ketamine being used to treat depression is,
after doing it weekly for about 4 or 5 months ive noticed ive started to suffer some of the bladder issues.

Ive never consumed more than 1 gram a week, ever.

I think its just the constant flow of ketamine through the body, its not good for it.

Perhaps an IM dose of 100mg a week would be fine,
but i dont have access nor have i ever seen a vial.

 

[Amu]

http://www.ncbi.nlm.nih.gov/pubmed/19919593

"Both frequent and abstinent using groups showed increased depression scores over the 12 months."

Ketamine will indeed give us insight into the glutamate/NMDA system and depression, but I don't think it's a good treatment for depression, we need to find how to activate mTOR pathways selectively. It's a good back-up though, until we have better stuff available.

"These findings indicate that semantic memory impairments associated with recreational ketamine are reversible upon marked reduction of use; however, impairments to episodic memory and possibly attentional functioning appear long-lasting. In addition, schizotypal symptoms and perceptual distortions may persist after cessation of ketamine use. Ketamine users, or potential users, should be aware of the enduring effects of this drug on aspects of memory and subjective experience."

http://www.ncbi.nlm.nih.gov/pubmed/15500598

K-holing is an enjoyable experience though, everything remotely enjoyable seems to be impairing something, there's always piracetam, and sex?

Selective AMPA/NMDA/mGluRs/GABA/Nicotinic partial agonists and modulators are the future for pretty much everything, it'll take a few decades to have them available and cheap though

 

[arctica]

only problem with ketamine being used to treat depression is,
after doing it weekly for about 4 or 5 months ive noticed ive started to suffer some of the bladder issues.

Ive never consumed more than 1 gram a week, ever.

I think its just the constant flow of ketamine through the body, its not good for it.

Perhaps an IM dose of 100mg a week would be fine,
but i dont have access nor have i ever seen a vial.

Are you currently enrolled in one of the (official) studies or is this personal research? What kind of dosages are you taking, and I assume the ROA is oral? Thanks for posting the clinical trials link.

 

[atrollappears]

Selective AMPA/NMDA/mGluRs/GABA/Nicotinic partial agonists and modulators are the future for pretty much everything, it'll take a few decades to have them available and cheap though

*cringes at the thought of any sort of ionotropic glutamate agonist*
...is it even possible to have partial agonists at ligand-gated ion channels? What would they do, just let fewer ions in at a steady rate? Sounds like it would still severely impair the ability of glutamate to signal properly.
I agree with the metabotropic glutamate receptors though, those seem promising. Antagonists for the autoreceptor ones and agonists for the others, if I recall correctly, are very exciting.
And why a nicotinic partial agonist? Nicotine itself is not addictive when administered without an MAOI, such as those in tobacco smoke, including harman and norharman. Personally, I think nicotine is really overlooked therapeutically, because of the medical stigma of tobacco. And you see it in studies too, researchers always assume that nicotine's effect on expression of X receptor/transporter is the result of some sort of damage, whereas a study on citicoline will call the same pattern "neurotrophic" or something.

Edit: I stand corrected, seems that these partial agonists do exist and are very interesting xD sorry for talking out of my ass

 

[ebola?]

Insofar as I've used ketamine to treat depressive symptoms, the regimen that I employed was pretty different from recreational use. The idea was to maintain a threshold for 2-3 days (or rather the waking hours thereof), and this would prove an effective anti-depressant for 2-3 weeks. So the total level of intake would be about a gram per month, maybe a bit less. This low a level of dosing unlikely presented a significant 'kidney load' at any point.

*cringes at the thought of any sort of ionotropic glutamate agonist*
...is it even possible to have partial agonists at ligand-gated ion channels? What would they do, just let fewer ions in at a steady rate? Sounds like it would still severely impair the ability of glutamate to signal properly.

Firstly, and obviously, at no point would a full glutamate agonist be appropriate. You could have two basic types of partial agonists, a competitive agonist that binds at the same site as glutamate but with lower intrinsic activity, or an allosteric modulator that binds at an alternate site on the receptor, either changing the efficacy of glutamate's activity or changing the tendency for the receptor to take in ions. The latter type of activity would not impair glutaminergic function directly.

ebola

 

[atrollappears]

Firstly, and obviously, at no point would a full glutamate agonist be appropriate. You could have two basic types of partial agonists, a competitive agonist that binds at the same site as glutamate but with lower intrinsic activity, or an allosteric modulator that binds at an alternate site on the receptor, either changing the efficacy of glutamate's activity or changing the tendency for the receptor to take in ions. The latter type of activity would not impair glutaminergic function directly.

A wild troll appears xD you got it.
Yep after I read that post I ended up reading about partial agonists at the glycine site. Though I admit I don't know about how the NMDA receptor works on a molecular level, it just didn't seem intuitive that the NDMAR would be biologically hardwired to maintain a state that's only partially permeable to Ca2+ when the endogenous ligands seem to have a binary stop/go type action. I was unaware that glycine played a role as an endogenous modulator at a different site---that's really pretty interesting. And it makes perfect sense that it would be therapeutically viable, since the receptor still relies on glutamate for activation, which the glia so courteously clean up for us, and because of that it wouldn't even out the glutamatergic nerve impulses necessary for proper cognitive function. It makes me wonder what other receptors have the potential to be activated in new and potentially useful ways, what new sites or signal transduction pathways we have yet to discover :D

More relevant to the thread though, what is the differential effect of ketamine that apparently causes depression in recreational use?