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Don Lemon interrogates Elon Musk on depression, his 'prescription' ketamine use and Trump in interview that got him fired from X | Daily Mail Online
'There are times when I have a negative chemical state in my brain, like depression I guess, or depression that's not linked to any negative news, and ketamine is helpful for getting one out of a negative frame of mind,' he added.
When asked if he has ever 'abused' the tranquilizing drug, Musk continued: 'I don't think so... if you use too much ketamine you can't really get work done, and I have a lot of work.'
'It's a prescription from a real doctor, not a, you know...' he added, as the conversation stalled and became awkward.
'Putting in 16-hour days, that's normal for me, and it's rare for me to even take off a weekend day, so I don't really have a situation where I can be not mentally acute for an extended period of time.
Psychedelics Sync Neurons: A Glimpse into Consciousness & Psychosis - Neuroscience News
“A Polish researcher had observed similar waves after giving rats the anesthetic ketamine. The ketamine was given at a low dose so that the rats were conscious, and the equivalent dose in a human causes psychedelic experiences.
“The waves they saw were in more cognitive regions of the brain than in the rats with Parkinson’s, and the frequency was higher, but that still made us consider whether there were links between the two phenomena.
“Perhaps excessive brain waves in the motor regions of the brain cause motor symptoms, while excessive waves in cognitive regions give cognitive symptoms,” says Pär Halje, researcher in neurophysiology at Lund University.
Ketamine Acts Fast to Treat Depression and Its Effects Last, But How? - Neuroscience News
Ketamine produces rapid and robust antidepressant effects in depressed patients within hours of administration, often when traditional antidepressant compounds have failed to alleviate symptoms. We hypothesized that ketamine would translocate Gαs from lipid rafts to non-raft microdomains, similarly to other antidepressants but with a distinct, abbreviated treatment duration. C6 glioma cells were treated with 10 µM ketamine for 15 min, which translocated Gαs from lipid raft domains to non-raft domains. Other NMDA antagonist did not translocate Gαs from lipid raft to non-raft domains. The ketamine-induced Gαs plasma membrane redistribution allows increased functional coupling of Gαs and adenylyl cyclase to increase intracellular cyclic adenosine monophosphate (cAMP). Moreover, increased intracellular cAMP increased phosphorylation of cAMP response element-binding protein (CREB), which, in turn, increased BDNF expression. The ketamine-induced increase in intracellular cAMP persisted after knocking out the NMDA receptor indicating an NMDA receptor-independent effect. Furthermore, 10 µM of the ketamine metabolite (2R,6R)-hydroxynorketamine (HNK) also induced Gαs redistribution and increased cAMP. These results reveal a novel antidepressant mechanism mediated by acute ketamine treatment that may contribute to ketamine’s powerful antidepressant effect. They also suggest that the translocation of Gαs from lipid rafts is a reliable hallmark of antidepressant action that might be exploited for diagnosis or drug development.
