How to source? Ideally in time for my next TMS
I know TMS clinics including the veterans TMS one that uses
Pharia also uses it
. This one targets precuneus which declines most with aging and reduces ppl doomscrolling
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FYI if you’re asian you’re more likely to have less potent BDNF signalling due to the Met variant… (and this may predict reduced response to TMS)
Cycloserine is a prescription-only antibiotic (used mainly for multidrug-resistant tuberculosis), and its use as an NMDA-partial agonist adjunct in TMS (transcranial magnetic stimulation) is still experimental. You can’t legally “source” it yourself unless you’re part of a clinical trial or have a physician who can prescribe it off-label.
If you’re exploring it for enhancement of neuroplasticity during TMS, that’s being studied in research settings—usually at academic centers running protocols on “accelerated TMS” or exposure-therapy augmentation. The right way to access it would be:
Clinical trial route:
Search for “cycloserine AND TMS” on ClinicalTrials.gov to find ongoing or completed studies. You can contact the principal investigators (often psychiatry or neurology departments at research hospitals) and ask about enrollment or compassionate-use extensions.Medical supervision route:
A psychiatrist or neurologist overseeing your TMS can apply for off-label use. A compounding pharmacy could then legally prepare the small doses used for cognitive or exposure enhancement (typically <100 mg, far below TB doses).
Without that medical framework, purchasing it would be considered unsupervised use of a controlled antibiotic—legally risky and medically unsafe.Alternative legal adjuncts under study:
Agents like D-serine, sarcosine, or glycine-site modulators have similar NMDA-coagonist activity and are easier to obtain as research-grade supplements, though none should be combined with TMS without medical input.
Because ketamine doesn’t just “turn NMDA off.” It changes the network state in a way that can prime plasticity.
Here’s the crisp version, without the fairy dust:
Disinhibition → glutamate burst
At sub-anesthetic doses, ketamine preferentially blocks NMDA receptors on fast-spiking GABA interneurons. Less inhibition on pyramidal cells means a transient surge of cortical glutamate, which drives AMPA currents. That burst is the opposite of “shutting the system down”; it’s a quick push that can amplify activity-dependent plasticity.AMPA up, BDNF up, mTOR on
The glutamate/AMPA drive triggers BDNF release and downstream mTORC1 signaling, which promotes new synapse formation and spine maturation over hours. Net effect: more synaptic “hardware” ready to be shaped by whatever patterned input comes next, including TMS.Metaplasticity (the BCM picture)
Plasticity has a sliding threshold. Briefly reducing NMDA signaling can lower the LTP threshold (or bias the system away from LTD), so the same TMS pattern produces a larger potentiation than it would in the baseline state. Ketamine isn’t the plasticity; it sets the stage for it.Not all NMDA is equal
Ketamine is an open-channel blocker with state, location, and subunit biases. Extrasynaptic NMDA signaling (often neurotoxic/depressogenic) may be damped more than synaptic NMDA needed for precise timing. Plus, ketamine touches other targets (HCN1, nAChRs, opioid tone) that tweak oscillations and excitability in ways that can facilitate TMS entrainment when dosed right.Metabolites matter
Certain metabolites (e.g., hydroxynorketamine isomers) enhance AMPA throughput with little direct NMDA blockade. That further tilts the balance toward potentiation windows where patterned stimulation bites harder.What this means for TMS, practically:
Dose and timing are everything. Too much ketamine or the wrong timing can blunt plasticity; low, well-timed dosing can open a plasticity window that TMS exploits.
Pattern matters. Theta-burst and other plasticity-heavy protocols seem more likely to benefit from a ketamine-primed state than plain high-frequency trains.
Do it in a clinic. You need vitals, seizure-risk screening, and someone who understands how to sequence infusion/intranasal dosing relative to TMS blocks.
So yes, ketamine antagonizes NMDA, but the network-level rebound and AMPA-BDNF cascade are why it can still boost the plastic effects you actually care about. It’s less “brake pedal” and more “tap the brake to downshift, then hit the gas at the right moment.”