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Posted by brk23 on January 12, 2014, at 17:03:51
Hey guys,for those who remember me its good to be back.If anyone wants any insight i can be googled brklyn23 i was a advid poster in a lot of groups like alt.ghb. alt.smart drugs etc.
Me and my girl have racked our brains trying to fight my severe treatment resistant depression.And for the most part we have made great strides.HOWEVER we never quite get "there"Well with the ketamine trials and other literature we have set our aim at NMDA ATGONISTS.
One reason why is waiting for ketamine got to me,so i legaly purchased a similar cousin drug MXE which was said to be actualy more potent.
Well let me tell you,for the first time in years i was cracking jokes non stop,laughing,i forgot what that was,also for those that care it took me into a spirtual stage where i felt connected but i wont get into that.
Anyway once this drug was discovered it was banned.Now im left with the memory of its beauty.
There was however a drug called AMANDATINE,i read on it and although its high for dopamine effects,it did have weak NMDA antagonist effects.I took two tabs which was all i had and felt super super calm.Im going to my doc tommorrow to ask on it.
Last there is a drug that is very potent at the NMDA site and even has been used off label for depression.
Its called rilutek.Problem is no docs seem to know of it,so theres no way theyll try it off label,also its EXPENSIVE around 900 dollers.
My question is has anyone used or heard of this drug with interest.?
Posted by Jeroen on January 14, 2014, at 12:21:01
In reply to Willyee ...NMDA ANTGONISTS., posted by brk23 on January 12, 2014, at 17:03:51
you better try minocycline which also works on glu1 or something and NMDA receptor
i tried amantadine for a week and got better but also got psychosis symptoms so i quit it on time
good luck
Posted by phidippus on January 18, 2014, at 2:35:43
In reply to Willyee ...NMDA ANTGONISTS., posted by brk23 on January 12, 2014, at 17:03:51
I take Rilutek. It has helped with both my OCD and my depression.
The mechanism of action of riluzole in the nervous system is complex. A considerable number of actions have been demonstrated in vitro, but some of these may have little relevance in vivo, where much lower concentrations of riluzole are achieved. Pittenger and colleagues have recently reviewed the subject very capably (Pittenger et al. 2008b).
Riluzole inhibits the release of glutamate at the presynaptic nerve cell terminus, most likely by blockade of voltage-gated sodium channels, and this effect may be achieved at low riluzole concentrations (demonstrated most recently by Urbani and Belluzzi 2000). It also likely reduces glutamate neurotransmitter vesicle fusion with the presynaptic cell membrane, either directly by opening voltage-gated calcium channels (Wang et al. 2004) or indirectly by altering G-proteinmediated signaling (Huang et al. 1997). Riluzole's effects on potassium channels have also been measured, but possibly not at clinically meaningful riluzole concentrations (Ahn et al. 2005; Mathie and Veale 2007).
Downstream effects of riluzole have been noted as well, but clinical significance remains unclear. These effects are stimulation of growth factor synthesis, including brain-derived neurotrophic factor (Fumagalli et al. 2006), and promotion of neuritogenesis, neurite branching, and neurite outgrowth (Shortland et al. 2006).
Riluzole has not been found to interact with any glutamate receptors at clinically meaningful concentrations (Habibi-Asl et al. 2009). However, enhancement of the hippocampal α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) glutamate receptor (GluR1, GluR2) subunit expression (Du et al. 2006) has been noted. And at high concentrations, there has been measured antagonism of AMPA and N-methyl-d-aspartate (NMDA) receptors (Pittenger et al. 2008b). Riluzole increases glial glutamate reuptake, possibly at the low levels found only extrasynaptically (Frizzo et al. 2004; Fumagalli et al. 2008).
In a recent study, riluzole (4 mg/kg, a reasonable dose when used in humans) attenuated the behavioral effects of chronic unpredictable stress, a rodent model of depression (Banasr et al. 2010). In the same study, the investigators demonstrated that metabolic and mRNA expression effects of stress were also attenuated by riluzole. These results are consistent with the evidence for the riluzole-enhanced reuptake of glutamate by glial cells. In addition, riluzole (10 μM) has been shown to exhibit a neuroprotective effect on rat glial cells to which a toxic level of glutamate (100 μM) was added in culture (Dagci et al. 2007).
There have been reports of riluzole effects on other neurotransmitters, but there has been little replication of these findings so far.
Eric
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