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Friday, November 13, 2015

Understanding Methamphetamine's effects on Neurotransmitters




Methamphetamine has the following Mechanism/s of Action.

  • TAAR1 Activation (Trace-Amine-Associate-Receptor-1) (increases cAMP)
  • Alpha-2-Adrenergic Agonist (decreases norepinephrine in some areas/brain region)
  • VMAT2 Inhibition  (affects 'recycling' of neurotransmitters)
  • Inhibits DAT, SERT, and NET by TAAR1 Activation (reverses monoamine transporters)
  • Increases dopamine and noradrenaline as well as serotonin by mechanism above.
  • Causes increase in glucose uptake.
  • Increases metabolism and thyroid hormones short-term.
  • Affects Insulin release by interacting with central monoamine systems.


A DEEPER OVERVIEW INTO METHAMPHETAMINE'S ACTIONS IN THE BRAIN AND CNS

Meth has a primary action of activating the Trace-Amine-Associated-Receptor; an action which leads to a rapid increase in the second messenger cyclic adenosine monophosphate - this messenger then activates an enzyme called  PROTEIN KINASE A - which then allows the reversal of transporters for monoamines (DAT, SERT , NET) - in a way, meth would be alike Cocaine, except it has a much longer duration of action ...up to 72 hours in some cases depending on method of administration and form used.

However, even though methamphetamine increases serotonin, dopamine and norepinephrine - it does so by bypassing direct inhibition of the transporters; so it wouldn't be exactly like amineptine, an SSRI and effexor for example - those three drugs combine would offer similar effects..but methamphetamine is indiscriminative so the effects happen to be largely 'perfectly equalized' - the effects on second messenger systems allow for a temporary boost in dopamine synthesis as well (increasing the body's natural dopamin production) - however, in the long-term - methamphetamine can damage dopamine neuron containing networks - by flooding the synapses repeatedly the result is dopamine receptor downregulation and internalization...additionally - excessive serotonin release blunts dopamine activity - leading to a downregulation in dopamine signaling.




Hence the performance of this study....



Because of that study - it is plausible and an acceptable resolve to use something like Amisulpride at LOW DOSES to augment methamphetamine's actions....however, meth still causes other issues long-term so my recommendation is something more like SELEGILINE in place of meth..selegiline in contrast is NEUROPROTECTIVE (protects brain cells and tissues) and raises dopamine by preventing it's breakdown - without having any effect on serotonin and only a minimal effect on adrenaline neurohormones.

If your goal is to reap the aphrodisiac benefits of amphetamine - there are much more effective substances for this purpose - one's with less incidence of adverse effects and more study in this specific area of research. 

Stuff like PT-141 and Masteron (for men) are a lot more effective. PT-141 rapidly increases libido in both men and women, whereas masteron increases erection quality and libido in men as well as aggression and strength.





**SOURCES/CITATIONS**





Methamphetamine-Induced Rapid and Reversible Changes in Dopamine Transporter Function: An In Vitro Model



https://books.google.com/books?id=ihxyHbnj3qYC&pg=PA421&lpg=PA421&dq=Methamphetamine+stimulates+noradrenergic+neurons&source=bl&ots=i8TL0Tcjsb&sig=Vfc6nGLNXEdhlSP2l7bhrQ4lz8I&hl=en&sa=X&ei=w_aOVcH9GsWrogT4-KygCg&ved=0CD8Q6AEwAw#v=onepage&q=Methamphetamine%20stimulates%20noradrenergic%20neurons&f=false

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2996466/
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3031865/

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