More evidence for the effects of an anti-depressant that can really affect sufferers of ‘treatment-less’ depression has been uncovered by clinical trials, headed by Dr Carlos Zarate, for the National Institute of Health earlier this year. The drug known affectionately as AZD6765 works by blocking the binding of the neurotransmitter glutamate at the NMDA receptors located upon the neurons within nerve cells. The NMDA receptors are the site of action for many psychotropic substances, including hallucinatory drugs such as ketamine. I have discussed the technical side of ketamine in my article The Action of Ketamine on Brains & Society in the Psychedelic Press UK. AZD6765 works in the exact same way as ketamine but with less things people may describe as ‘side-effects’ – depending on your views or mindset, the term ‘adverse’ or ‘propitious’ could proceed here to help us penetrate to the essentials – in this case, the ambiguous term ‘less side-effects’ translates into a reality of ‘less psychotropic effects’. In a clinical sense this is advantageous for the treatment of clinically depressed patients. One does not need to be an objective bystander remotely viewing oneself, surrounded by unfolding chrome volumetric curves, if all one wishes to do is muster the courage to go outside for some groceries.

Ketamine can also give what doctors call a ‘residual anti-depressant effect’ for up to a week after the original dose. A ‘residual anti-depressant effect’ can be explained with terms akin to a ‘warm afterglow’. This psychosomatic ‘warmth’ that is so often experienced in the days after a session using certain compounds, in particular psychedelic psychoactives. AZD6765 has been shown to give a ‘residual anti-depressant effect’ for merely two days after procurement. It also allows for a rapid onset of effects, between 1-2 hours, according to the trials, and helps to eliminate severe depression for up to 30 minutes. So what we seem to have here is a ‘ketamine light’. Dr Carlos Zarate’s trials revealed that only 32% of the patients tested showed an anti-depressant response to the drug, compared to 52% of the same patients registering meaningful anti-depressant responses to ketamine. The figure of 32% is still significant enough to be above the expected result for a placebo, so the work in general can be seen as encouraging. Such encouragement is derived from the progress in development of ‘glutamate blocker based’ anti-depressants in the treatment of clinically depressed patients who have grown immune to benzodiazepine derivatives. Further studies on AZD6765 are ongoing, especially in regards to the effects of acute and chronic dosage within fixed periods of time. It’s only a matter of time before we should start to see major elaborations on and within the treatment of depression, in regards to non-benzodiazepine based anti-depressants, which haven’t exactly dominated psychiatry and the pharmaceutical industry over the past 40 years.

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