What country do you live in? I'm also interested in getting a prescription for Deprynl for the same reasons you mention and I'm seeing my psychiatrist on Thursday. Do you take any current prescription medication?
My Jumex deprenyl just got here today from BioGenesis (https://www.biogenesis-antiaging.com). I am 20 and ordered the deprenyl for the same reasons as mentioned. Another member on these forums told me that Deprenyl could actually decrease long term dopamine production: "Be careful with deprenyl. Chronic use lowers tyrosine hydroxylase so you'll have absolutely NO dopamine production. If you do decide to use it, don't go above 1 drop a week. Trust me on this. To raise dopamine, I found that manganese and tyrosine work very, very well. So well, that I don't feel the depression I used to get with choline supplements. You could try that.."
Anyways, I'm putting the deprenyl, hydergine, and pregnenolone that I received today on hold until I get more green lights... or I become desperate.
this is a little scary. i couldn't find the post you were talking about (could you link me?) but i did find some abstracts on the subject. i think that the user quoted above may be misinterpreting the studies a bit.
Reduced striatal tyrosine hydroxylase activity is not accompanied by change in responsiveness of dopaminergic receptors following chronic treatment with deprenyl
Deprenyl is the only selective monoamine oxidase B (MAO-B) inhibitor that is in clinical use for the treatment of Parkinson's disease. Our previous studies showed that chronic treatment of rats with low (MAO-B selective) doses of deprenyl inhibited dopamine (DA) re-uptake and enhanced DA release in the striatum. These changes could affect DA synthesis rate by activation of negative feedback loops. Chronic deprenyl treatment has also been suggested to cause down-regulation of release-modulating DA receptors. The effects of chronic and acute treatment with deprenyl on ex vivo striatal tyrosine hydroxylase activity were therefore studied, by determination of steady-state tissue level of DOPA following administration of NSD-1015 (100 mg/kg i.p.). In addition, we assessed changes in the in vivo sensitivity of dopaminergic receptors from the reduction in DOPA extracellular level after systemic apomorphine administration (2.5 mg/kg s.c.), following elevation of microdialysate DOPA by systemic or local aromatic amino acid decarboxylase inhibition with NSD-1015. Chronic treatment with deprenyl (0.25 mg/kg s.c. daily for 21 days) caused a significant reduction in tyrosine hydroxylase activity to 60% of control, with no change in the apomorphine-induced reduction of microdialysate DOPA and DOP AC. The reduction in tyrosine hydroxylase activity is compatible with our previous results showing an increase in striatal DA extracellular level following chronic treatment with deprenyl. The increased extracellular striatal DA level could reduce tyrosine hydroxylase activity through activation of a negative feedback loop, by activation of either presynaptic or postsynaptic DA receptors.
the stuff here about negative feedback loops isn't making a whole lot of sense to me, but what i'm gathering from this study is that tyrosine hydroxylase is being reduced as a sort of compensatory mechanism. that is, tyrosine hydroxylase production doesn't need to be anywhere near as high since mao-b is inhibited and there is a whole lot of extra dopamine floating around. so when the stock of dopamine is high production (of TH) ceases. what worried me about that quote is that i feel like it might have implied that the drop in tyrosine hydroxylase was permanent or damaging. i don't think there is anything here to suggest this. the creation of TH will probably go right back up once the addition of deprenyl is removed. it's a homeostatic reaction that'll balance out either which way. you're still getting more dopamine despite the counterbalanced TH level. it's possible that i'm getting this study wrong, so anyone please feel free to chime in.
aside from this, i've found a couple of possibly contradictory studies which seem to suggest that deprenyl actually increases TH:
Résumé / Abstract
Chronic treatment of aged rats with deprenyl prevents age-induced protein oxidation in substantia nigra and protects tyrosine hydroxylase (TH) enzyme against inactivation [11]. With these precedents, we treated adult rats with deprenyl for 3 weeks in order to get further insight in the mechanism by which deprenyl exerts such actions. After completing the treatment, dopamine (DA) levels markedly increased in both striatum and substantia nigra while levels of the acid DA metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), decreased in the two brain areas, thus proving MAO-inhibiting properties of the treatment. We then studied the cellular expression of TH mRNA by in situ hybridization. Following treatment with deprenyl, levels of TH mRNA were significantly higher in individual dopaminergic nigral cell bodies than in those of control rats (+74%). Western blotting analysis of TH enzyme amount revealed a positive effect of the treatment in both the terminal field (+44%) and the cell body region (+31%). This correlation between TH mRNA and amount was also extended to TH enzyme activity in the two brain areas studied, which significantly increased in striatum (+57%) and substantia nigra (+35%) following deprenyl treatment. Taken together, our results clearly suggest a TH-inducing effect of deprenyl in the dopaminergic nigrostriatal system, which seems to be independent of its protective action against oxidative stress described previously. These results expand out knowledge about the beneficial effect of deprenyl in the therapy of Parkinson's disease.
We studied the effects of treatment with (-)-deprenyl, a monoamine oxidase B inhibitor, on plasma levels of insulin-like growth factor-I (IGF-I) (as indicator of growth hormone (GH) secretion), levels of monoamines and their metabolites, and the activity and content of tyrosine hydroxylase - the rate-limiting enzyme in the biosynthesis of catecholamines - in the hypothalamus and hypophysis of old male rats. Male Wistar rats (22 months old) were treated with 2 mg deprenyl/kg body weight s.c. three times a week for 2 months. At the end of the treatment period, blood was collected for measurement of plasma IGF-I levels by radioimmunoassay (RIA). The concentrations of dopamine, serotonin (5-HT) and their main metabolites were determined by high performance liquid chromatography (HPLC) with electrochemical detection, and the tyrosine hydroxylase content in hypothalamus and hypophysis was determined by enzyme-linked immunoabsorbent assay (ELISA). (-)-Deprenyl treatment produced a pronounced increase in dopamine and 5-HT in both the hypothalamus and hypophysis (P < 0.01). The main dopaminergic metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), decreased in hypothalamus but not in hypophysis, and treatment had no effect on the concentration of 5-hydroxyindole-3-acetic acid (5-HIAA). The tyrosine hydroxylase activity and tyrosine hydroxylase content increased in hypothalamus and hypophysis (P < 0.05). In the hypophysis the increase in tyrosine hydroxylase activity was consistent with the increase in tyrosine hydroxylase amount. Moreover, (-)-deprenyl treatment restored the IGF-I plasma levels in old rats to a concentration similar to those found in young animals. Postulated anti-aging effects of (-)-deprenyl could hence be due to restoration of hypothalamic hormones such as GH.
i think we're at least in the clear on this point. would deprenyl be anywhere as close to as prevalent as it is on this forum or at all if that were true? that isn't even an age-dependent argument against it. dude sounds like he probably misinterpreted some stuff. i also find it hard to believe that tyrosine or manganese are going to do a whole lot of good. maybe in certain rare instances tyrosine may be of some help, but everything i've read suggests that if there are any benefits, they're basically short term. neither tyrosine nor manganese are going to come anywhere close to the therapeutic effect that drugs like deprenyl, amphetamines, DA reuptake inhibitors, etc are going to have.
Edited by brain, 16 September 2009 - 07:05 AM.
