3 ms·

lol, what? NMDA receptor agonists can be directly neurotoxic. See, e.g.: https://pubmed.ncbi.nlm.nih.gov/9109508/ https://pubmed.ncbi.nlm.nih.gov/9109508/ Al

lol, what? NMDA receptor agonists can be directly neurotoxic. See, e.g.: https://pubmed.ncbi.nlm.nih.gov/9109508/ https://pubmed.ncbi.nlm.nih.gov/9109508/ Also: https://www.mdpi.com/2039-4713/15/1/12 https://www.mdpi.com/2039-4713/15/1/12 > "Normal NMDA receptor (NMDAR) function is essential for neuronal development and higher brain functionality, while its inappropriate stimulation results in neurological deficits."

johnisgood 2y ago
I made a typo, it is a NMDA receptor antagonist. Additionally, I can find sources supporting my claim, too. > Results in rodent models indicate that a single dose of ketamine induces robust markers of neuroplasticity in depression-relevant brain regions, including increased BDNF release and the stimulation of mTOR signaling in the PFC [23, 24]. In addition, ketamine induces an increase in synapse number and function in the PFC, reversing the loss of specific synapses by stress, an effect that seems necessary for the persistence of its antidepressant-like behavioral effects.[1] [1] https://www.nature.com/articles/s41398-023-02451-0 https://www.nature.com/articles/s41398-023-02451-0 From Wikipedia: > Ketamine is under investigation for its potential in treating treatment-resistant depression. Ketamine is a known psychoplastogen, which refers to a compound capable of promoting rapid and sustained neuroplasticity. Additionally: https://www.resetketamine.com/blog/2021/6/2/ketamine-and-its-neuroplastic-effect-on-the-brain https://www.resetketamine.com/blog/2021/6/2/ketamine-and-its... Additionally #2: https://pmc.ncbi.nlm.nih.gov/articles/PMC8190578/ https://pmc.ncbi.nlm.nih.gov/articles/PMC8190578/ Additionally #3: https://www.sciencedirect.com/science/article/abs/pii/S0165614721001577 https://www.sciencedirect.com/science/article/abs/pii/S01656... > Ketamine (NMDAR antagonism) and classical psychedelics (5-HT2AR agonism) trigger a long-lasting state of enhanced glutamate-driven neuroplasticity in frontocorticolimbic pyramidal neurons.
- TeaBrain 2y ago
  Your counterclaim is based on the unsupported assumption that a substance having relatively high neurotoxic potential means that it cannot induce neuroplasticity. The two are not mutually exclusive, and in the case of the substance in question, it is well known to have both high neurotoxic potential, as all strong NMDA antagonists do, as well as the ability to induce increased neuroplasticity.
  - johnisgood 2y ago
    Yes, you are pretty much correct.

johnisgood 2y ago

I made a typo, it is a NMDA receptor antagonist. Additionally, I can find sources supporting my claim, too. > Results in rodent models indicate that a single dose of ketamine induces robust markers of neuroplasticity in depression-relevant brain regions, including increased BDNF release and the stimulation of mTOR signaling in the PFC [23, 24]. In addition, ketamine induces an increase in synapse number and function in the PFC, reversing the loss of specific synapses by stress, an effect that seems necessary for the persistence of its antidepressant-like behavioral effects.[1] [1] https://www.nature.com/articles/s41398-023-02451-0 https://www.nature.com/articles/s41398-023-02451-0 From Wikipedia: > Ketamine is under investigation for its potential in treating treatment-resistant depression. Ketamine is a known psychoplastogen, which refers to a compound capable of promoting rapid and sustained neuroplasticity. Additionally: https://www.resetketamine.com/blog/2021/6/2/ketamine-and-its-neuroplastic-effect-on-the-brain https://www.resetketamine.com/blog/2021/6/2/ketamine-and-its... Additionally #2: https://pmc.ncbi.nlm.nih.gov/articles/PMC8190578/ https://pmc.ncbi.nlm.nih.gov/articles/PMC8190578/ Additionally #3: https://www.sciencedirect.com/science/article/abs/pii/S0165614721001577 https://www.sciencedirect.com/science/article/abs/pii/S01656... > Ketamine (NMDAR antagonism) and classical psychedelics (5-HT2AR agonism) trigger a long-lasting state of enhanced glutamate-driven neuroplasticity in frontocorticolimbic pyramidal neurons.

TeaBrain 2y ago
Your counterclaim is based on the unsupported assumption that a substance having relatively high neurotoxic potential means that it cannot induce neuroplasticity. The two are not mutually exclusive, and in the case of the substance in question, it is well known to have both high neurotoxic potential, as all strong NMDA antagonists do, as well as the ability to induce increased neuroplasticity.
- johnisgood 2y ago
  Yes, you are pretty much correct.