I'm surprised no one has brought up the study reviews on Chemically Correct at M&M, as they kick a lot of ass. Here they are, for Deprenyl:
http://www.mindandmu...-andrew-novick/http://www.mindandmu...-andrew-novick/... but all of them are recommended reading.
Honestly, the most interesting thing I've taken from these articles is something that hasn't been brought up clearly yet in this thread: Low-Dose Deprenyl.
From Chemically Correct:
L-deprenyl increases levels of the enzyme L-amino acid decarboxylase, a necessary enzyme for monoamine synthesis (23). Its effect on tyrosine hydroxylase, the rate limiting factor for dopamine synthesis, is variable. 2mg/kg of l-deprenyl given 3 times a week for 2 months increases tyrosine hydroxylase expression (27). However, repeated dosages of 10mg/kg of l-deprenyl decreased tyrosine hydroxylase (28). Chronic treatment with .25mg/kg for 21 days reduced tyrosine hydroxlase activity to 60% of the control group (31). Another group of researchers showed .1mg/kg for 21 days caused reduced tyrosine hydroxylase activity at first, but activity recovered by day 14 and increased after day 21 (32). While these results seem contradictory, it does appear that low, chronic doses of l-deprenyl are more likely to increase tyrosine hydoxylase activity than higher acute doses.
23. Li XM, Juorio AV, Qi J, Boulton AA. L-deprenyl induces aromatic L-amino acid decarboxylase (AADC) mRNA in the rat substantia nigra and ventral tegmentum. An in situ hybridization study. Mol Chem Neuropathol. 1998 Aug-Dec;35(1-3):149-55.
27. De la Cruz CP, Revilla E, Rodriguez-Gomez JA, Vizuete ML, Cano J, Machado A. (-)-Deprenyl treatment restores serum insulin-like growth factor-I (IGF-I) levels in aged rats to young rat level. Eur J Pharmacol. 1997 May 30;327(2-3):215-20.
28. Fowler JS, Volkow ND, Logan J, Franceschi D, Wang GJ, MacGregor R, Shea C, Garza V, Pappas N, Carter P, Netusil N, Bridge P, Liederman D, Elkashef A, Rotrosen J, Hitzemann R. Evidence that L-deprenyl treatment for one week does not inhibit MAO A or the dopamine transporter in the human brain. Life Sci. 2001 May 4;68(24):2759-68.
31. Lamensdorf I, Finberg JP. Reduced striatal tyrosine hydroxylase activity is not accompanied by change in responsiveness of dopaminergic receptors following chronic treatment with deprenyl. Neuropharmacology. 1997 Oct;36(10):1455-61.
32. Vrana SL, Azzaro AJ, Vrana KE. Chronic selegiline administration transiently decreases tyrosine hydroxylase activity and mRNA in the rat nigrostriatal pathway. Mol Pharmacol. 1992 May;41(5):839-44.
So it's perfectly possible to trick one's body into upregulating Tyrosine Hydroxylase rather than downregulating it. My question are if this is qualitatively different from taking higher-dose deprenyl, which increases dopamine levels by other means. DevinThayer, you mentioned before that l-phenylethylamine would technically help your brain have more dopamine, but it made you silly; if it counts for
how dopamine is raised, or
where, then increased tyrosine hydroxylase expression could be a completely different ball game.
(You'd probably end up with something in line with
aLurker's insomnia and energy catapults, but it's still moot.)
