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How to reverse Dopamine tolerance effects from CDP, Uridine

cdp uridine tolerance virus influenza dopamine receptor density sam-e

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#1 permhealing

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Posted 30 September 2015 - 12:51 AM


Hi Everyone,

 

I would like some advice on how to go forward with my brain healing.

 

So around late 2012 I tried Sam-E as I was getting some pleasure, interest in food, sex, but not much for motivation, career, thinking it would boost dopamine and motivation.  Although it did make me more focused on career, it also gave me plenty of paranoia, ocd, and later on severe anxiety, harder to digest foods, frequent sinus infections, much less interest in food, and less into sex, more concerned with morality.

 

So I took it for about 8 months before I stopped it.  What happened afterwards was that it left me with a weaker immune system where I would be getting frequent sinus infections, and influenza (freezing cold, spleen area pain, which was confirmed in blood tests).

 

It wasn't until late July 2015 that I came out of the paranoia induced by sam-e to be comfortable to try out some brain supplements (previously paranoid of any side effects from taking anything).  I first tried Mucuna Pruriens min. 15% l-dopa in small doses and the first few days my body temp was so much warmer, and my mood was pumped.

 

This was great as it helped solve my virus (freezing) problems.  I believe the virus was caused by my insufficient dopamine affecting my immune system.  I then read about Uridine and how it could heal dopamine receptor density or damage and that how CDP Choline also contained uridine so I proceeded to try that.  During the initial 2 days I would feel a surge in libido and pumped mood, but also followed by a worse sinus infection (week at home), and then also depression.  I would also need to take higher amounts of the MP to attain the same effects as before I started CDP.  And if I didnt take higher doses of MP I would get the old freezing, cold hands, feet, and virus fatigue symptoms.

 

Therefore I think the CDP or uridine inside it caused dopamine tolerance maybe by increasing the receptor density.  I am not comfortable with taking high doses of MP now as it can cause anxiety and insomnia.

 

 

Short Question:

 

So as my main priority now is to minimise the sinus and virus occurence, do you think I should try to decrease dopamine receptor density so that just small doses of MP would have effects?

 

And if so, what ways are there to decrease dopamine receptor density?



#2 addforever

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Posted 30 September 2015 - 05:16 PM

increased dopamin receptor density does not cause dopamin tolerance.it actually lowers the tolerance.
using L-Dopa might lowers it.
one more thing: L-Dopa has presystemic elimination in the enterocytes (intestinals). thats why in parkinsons disease L-dopa is combinated with COMT inhibitors.

I got one question: do you use B6 vitamin?

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#3 permhealing

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Posted 01 October 2015 - 12:47 AM

increased dopamin receptor density does not cause dopamin tolerance.it actually lowers the tolerance.
using L-Dopa might lowers it.
one more thing: L-Dopa has presystemic elimination in the enterocytes (intestinals). thats why in parkinsons disease L-dopa is combinated with COMT inhibitors.

I got one question: do you use B6 vitamin?

 

ok so in theory CDP should have helped, but for me it led to depression and worse dopamine status after the initial spikes, where I would have to increase the dose of MP alot to get the earlier benefits.

 

I don't use inhibitors like green tea because I could feel the mental benefits from MP alone.

 

And I also don't use B6 as I read in some MP supplement instructions to avoid using it.

 

What does it do?  If it helps and doesn't increase noradrenaline or anxiety I might try it.



#4 permhealing

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Posted 01 October 2015 - 12:52 AM

Just to rephrase my earlier question:

 

Would anyone know why I experienced tolerance to Mucuna and depression, worse dopamine status after using CDP Choline?

 

I have used Alpha GPC before CDP and didn't get much negative effects.



#5 gamesguru

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Posted 01 October 2015 - 01:21 AM

Mucuna contains natural l-dopa, which over time in large quantities, can cause generalized, systemic dopamine downregulation.

 

CDP-choline is decomposed in the brain to choline + cytidine.  The cytidine is then metabolized to uridine, which affects a dopamine release.  Now it's unclear whether long-term this affects a systemic upregulation or downregulation on dopamine reactivity.

I think short-term it will increase activity via increased release, followed by a brief period where the receptors downregulate (calm before the storm), leading to a depletion of dopamine (due to sustained release), which in turn will finally affect an upregulation of receptors and reactivity to above baseline.  Just a guess, could be mistaken.  If it does downregulate long-term, that would fit in accordance with your anecdote.

It also promotes neurite outgrowth, which doesn't sound too shabby.

Dietary uridine-5′-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats
Membrane phospholipids like phosphatidylcholine (PC) are required for cellular growth and repair, and specifically for synaptic function. PC synthesis is controlled by cellular levels of its precursor, cytidine-5′-diphosphate choline (CDP-choline), which is produced from cytidine triphosphate (CTP) and phosphocholine. In rat PC12 cells exogenous uridine was shown to elevate intracellular CDP-choline levels, by promoting the synthesis of uridine triphosphate (UTP), which was partly converted to CTP. In such cells uridine also enhanced the neurite outgrowth produced by nerve growth factor (NGF). The present study assessed the effect of dietary supplementation with uridine-5′-monophosphate disodium (UMP-2Na+, an additive in infant milk formulas) on striatal dopamine (DA) release in aged rats. Male Fischer 344 rats consumed either a control diet or one fortified with 2.5% UMP for 6 wk, ad libitum. In vivo microdialysis was then used to measure spontaneous and potassium (K+)-evoked DA release in the right striatum. Potassium (K+)-evoked DA release was significantly greater among UMP-treated rats, i.e., 341±21% of basal levels vs. 283 ± 9% of basal levels in control rats (p<0.05); basal DA release was unchanged. In general, each animal’s K+-evoked DA release correlated with its striatal DA content, measured postmortem. The levels of neurofilament-70 and neurofilament-M proteins, biomarkers of neurite outgrowth, increased to 182±25% (p<0.05) and 221 ± 34% (p<0.01) of control values, respectively, with UMP consumption. Hence, UMP treatment not only enhances membrane phosphatide production but also can modulate two membrane-dependent processes, neurotransmitter release and neurite outgrowth, in vivo.
 

https://books.google...AAQBAJ&pg=PA414

 

 

You could also try ginseng or st. johns, both inhibitors of dopamine-Beta-hydroxylase (which degrades DA→NE).

Antidepressant-like effects of Trichilia catigua (Catuaba) extract: evidence for dopaminergic-mediated mechanisms

  • Acute oral treatment with the extract of T. catigua produced antidepressant-like effects in the forced swimming model in both mice and rats. Anti-immobility actions of T. catigua extract in mice were significantly reversed by haloperidol or by chlorpromazine, but not by pimozide, ketanserin, spiroxatrine or p-chlorophenylalanine. In vitro, T. catigua extract concentration-dependently inhibited the uptake and increased the release of serotonin, and especially of dopamine, from rat brain synaptosomal preparations.

Mucuna[1]

Rhodiola (MAO-B)

^^^all these things I suspect increase dopamine levels and decrease dopamine receptors

------------------

these are more natural choices, favoring homeostasis and equilibrium (pay special attention to the upregulators of DA receptors)

PKU-Food-Diagram-copy.jpg
Inducers of PH (phenylalanine hydroxylase):

Lamiaceae[1]??

Simple diet[2]

Exercise[3]

Iron[4]

High ORAC foods[5]

 

Inducers of TH (tyrosine hydroxylase):

Horny goat weed[1]

Lithium

Ginkgo

Bacopa[2]

Green tea[3]

 

Upregulators of receptors (dopamine):

Caffeine[1]

Bacopa[2]

Exercise[3]

Antidepressants[4], [5]

 


Edited by gamesguru, 01 October 2015 - 01:26 AM.

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#6 permhealing

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Posted 02 October 2015 - 01:05 PM

 

Mucuna contains natural l-dopa, which over time in large quantities, can cause generalized, systemic dopamine downregulation.

 

CDP-choline is decomposed in the brain to choline + cytidine.  The cytidine is then metabolized to uridine, which affects a dopamine release.  Now it's unclear whether long-term this affects a systemic upregulation or downregulation on dopamine reactivity.

I think short-term it will increase activity via increased release, followed by a brief period where the receptors downregulate (calm before the storm), leading to a depletion of dopamine (due to sustained release), which in turn will finally affect an upregulation of receptors and reactivity to above baseline.  Just a guess, could be mistaken.  If it does downregulate long-term, that would fit in accordance with your anecdote.

It also promotes neurite outgrowth, which doesn't sound too shabby.

 

 

Thanks for your advice.

 

I will actually try uridine on itself some time later to rule out choline actually causing the depression.

 

I will also try the SJW if the anxiety gets any worse.

 

 

 



#7 gamesguru

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Posted 02 October 2015 - 01:20 PM

For anxiety also near the top of the list are

Theanine/green tea, ginkgo, ginseng, ALCAR/PS, bacopa, kava, ash, valerian

 

Area pointed out that wheat also inhibits dopamine-beta-hydroxylase, and that inositol and forskolin also upregulate dopamine receptors (D2 iirc).

0009155_food-for-life-ezekiel-7-grain-whUnsalted_Build__merged___skewed_.jpg

note the magnesium content on the sprouted bread...

IMG_2533.jpg


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#8 permhealing

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Posted 05 October 2015 - 10:56 AM

 

 

 

Thanks alot,

 

I will try out a few things.  I won't try theanine though because I read that it could increase methylation.



#9 gamesguru

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Posted 05 October 2015 - 02:01 PM

Trust me the theanine is such a weak overmethylator, the EGCG is gonna dominate, and leave you balanced, perhaps undermethylated.

Green tea also inhibits acetylation and deacetylation.  Also: https://www.google.c...Phosphorylation

Table 1

Common HDAC, HAT and DNMT modulators derived from natural sources

 
HDAC    Allyl mercaptan Nian et al. (2008) EGCG Thakur et al. (2012) Amamistatin Fennell and Miller (2007)  Apicidin Darkin-Rattray et al. (1996)  Azumamide E Maulucci et al. (2007)  Caffeic acid Waldecker et al. (2008)  Chlamydocin Brosch et al. (1995)  Chlorogenic acid Bora-Tatar et al. (2009)  Cinnamic acid Bora-Tatar et al. (2009)  Coumaric/hydroxycinnamic acid Waldecker et al. (2008)  Curcumin Bora-Tatar et al. (2009)  Depudecin Kwon et al. (1998)  Diallyl disulfide Lea et al. (1999)  Equol Hong et al. (2004)  Flavone Bontempo et al. (2007)  Genistein Kikuno et al. (2008)  Histacin Haggarty et al. (2003)  Isothiocyanates Ma et al. (2006)  Largazole Ying et al. (2008)  Pomiferin Son et al. (2007)  Psammaplin Pina et al. (2003)  SAHA (Vorinostat) Richon et al. (1998)  S-allylmercaptocysteine Lea et al. (2002)  Sulforaphane Myzak et al. (2004)  Trapoxin (Kijima et al. 1993)  Ursolic acid Chen et al. (2009)  Zerumbone Chung et al. (2008)
 
HAT  Allspice Lee et al. (2007)  Anarcardic acid Balasubramanyam et al. (2003), Ghizzoni et al. (2010)  EGCG Choi et al. (2009a)  Curcumin Balasubramanyam et al. (2004), Marcu et al. (2006)  Gallic acid Choi et al. (2009b)  Garcinol Balasubramanyam et al. (2004)  Quercetin Ruiz et al. (2007)  Sanguinarine Selvi et al. (2009)  Plumbagin Ravindra et al. (2009)
 
DNMT  Genistein Day et al. (2002)  EGCG Fang et al. (2003)  Psammaplins Pina et al. (2003)  Quercetin, fisetin, myricetin Lee et al. (2005)  Caffeic acid Lee and Zhu (2006)  Chlorogenic acid Lee and Zhu (2006)  Curcumin Moiseeva et al. (2007)  Parthenolide Liu et al. (2009)  Mahanine Sheikh et al. (2010)

SAHA Suberoylanilide hydroxamic acid, EGCG epigallocatechin gallate

 

 

I would recommend it in the form of tea:

post-13945-0-83913000-1444053215.jpg

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Edited by gamesguru, 05 October 2015 - 02:02 PM.

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#10 permhealing

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Posted 07 October 2015 - 01:05 AM

 

 

I actually tried some Alpha GPC over the weekend, and it actually helped alot with the tension.  But by the same token it also led to sinus infections.  Either it created too much choline in my body.  Or it decreased dopamine in my body, and that my already deficient dopamine status (less motivated, pleasure from things) increases my chances of infections.

 

Really regret taking Sam-e as it decreased my dopamine levels, leading to a structural deficit.

 

I also tried theanine daytime and it did make me sleepy afterwards.  Even more so than 5htp.

 

Next step would be to try out uridine on itself to hope that it decreases tolerance to dopamine or MP, but just hope that I don't experience the CDP caused depression I had weeks ago.

 

Another option would be to try higher % dopa forms of MP.

 

I also read that some people also get depression from uridine:

https://www.reddit.c...n_and_lethargy/



#11 gamesguru

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Posted 07 October 2015 - 02:00 AM

you could also have decreased D2/D3 (hyperdopamine), then something like caffeine (boosts D2/D3 receptors) may help, and dopamine boosters *cough* uridine *cough* may hurt (it could explain depressive anecdotes surrounding uridine).

anyways caffeine will help theanine not be so sedating.

 

as for choline and immune health, deficiency causes vagus nerve[!] miscommunication... very unlikely even high doses would affect the immune system, not before headache, sweating, and GI symptoms occured.

 

i found one study suggesting hyperdopamine impairs immune health, but i would guess your immunocompromisation has another cause (one not directly related to neurotransmitter systems, could be stress combined with unfavorable amino acid eg. lysine vs arginine).

Reduced splenic natural killer cell activity in rats with a hyperreactive dopaminergic system.


Edited by gamesguru, 07 October 2015 - 02:46 AM.

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#12 permhealing

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Posted 07 October 2015 - 10:33 AM

 

 

Did you mean I have reduced D2/D3 receptors, but excess dopamine neurotransmitters?

 

I thought that uridine doesn't really work on dopamine neurotransmitters but more works on dopamine receptors and its density?



#13 gamesguru

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Posted 07 October 2015 - 05:17 PM

Yes, the less receptors: the less autoreceptors and the more neurotransmitter release (hyperdopamine).  If receptors & autoreceptors go up, neurotransmitters go down (hypodopamine).  My study [there are conflicting or incongruent ones] suggests uridine increases dopamine release (hyper), thereby desensitizing D2/D3.

 

Out of good taste, I've included the incongruent findings/conflicting studies:

 Effects of chronic treatment with uridine on striatal dopamine release and dopamine related behaviours in the absence or the presence of chronic treatment with haloperidol.
Uridine (15mg/kg/day, i.p.), haloperidol (1mg/kg/day, i.p.), uridine (15mg/kg/day, i.p.) plus haloperidol (1mg/kg/day, i.p.) or saline have been chronically administered to Sprague-Dawley male rats. Following 1 week of wash-out, the effects of these treatments on basal striatal dopamine (DA) release as well as on the DA release induced by an acute haloperidol challenge (2mg/kg, i.p.) were studied by means of intracerebral microdialysis. Behavioural tests such as haloperidol-induced catalepsy or apomorphine-induced stereotypics were also performed 4-7 days after drug withdrawal. The chronic treatment with uridine alone or associated with haloperidol markedly reduced DA release induced by an acute haloperidol challenge. The behavioural studies also indicated a change in DA-related behaviours in these conditions. The animals chronically treated with uridine showed significant increases in the stereotypy scores and in the catalepsy induced by an acute haloperidol challenge with respect to saline treated rats. The present results indicate that a chronic uridine treatment is able to potentiate the reduction of the striatal DA transmission induced by acute and chronic haloperidol treatment. This finding suggests the possibility to reduce the neuroleptic dose in the treatment of schizophrenia by combining neuroleptic and uridine treatments, thus making it possible to relieve some of the side effects of neuroleptic therapy.

 

Dietary uridine-5'-monophosphate supplementation increases potassium-evoked dopamine release and promotes neurite outgrowth in aged rats.


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#14 permhealing

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Posted 11 October 2015 - 11:27 PM

 

 

 

If the main action of uridine is mostly to increase dopamine neurotransmitters, then why wouldn't one just try MP as it contains dopamine as well.  I still thought uridine was mostly considered for its effects on dopa receptors?

 

And for an ideal dopamine system, is it better to have more receptors and less neurotransmitters?



#15 gamesguru

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Posted 12 October 2015 - 12:34 AM

If the main action of uridine is mostly to increase dopamine neurotransmitters, then why wouldn't one just try MP as it contains dopamine as well.  I still thought uridine was mostly considered for its effects on dopa receptors?

 

And for an ideal dopamine system, is it better to have more receptors and less neurotransmitters?

 

On uridine: the only two studies are the ones I listed, and they say opposite things (one says increased dopamine release, the other says decreased).  The question is who will you choose to believe?

Well, just found a third study (1989, found via the book in my first post) is the only other I could find... so basically it's two studies against one.  66.7% chance you are right, it increases receptors, deceases transmitter.

Effects of chronic treatment with uridine on striatal dopamine release and dopamine related behaviours in the absence or the presence of chronic treatment with haloperidol.
Uridine (15mg/kg/day, i.p.), haloperidol (1mg/kg/day, i.p.), uridine (15mg/kg/day, i.p.) plus haloperidol (1mg/kg/day, i.p.) or saline have been chronically administered to Sprague-Dawley male rats. Following 1 week of wash-out, the effects of these treatments on basal striatal dopamine (DA) release as well as on the DA release induced by an acute haloperidol challenge (2mg/kg, i.p.) were studied by means of intracerebral microdialysis. Behavioural tests such as haloperidol-induced catalepsy or apomorphine-induced stereotypics were also performed 4-7 days after drug withdrawal. The chronic treatment with uridine alone or associated with haloperidol markedly reduced DA release induced by an acute haloperidol challenge. The behavioural studies also indicated a change in DA-related behaviours in these conditions. The animals chronically treated with uridine showed significant increases in the stereotypy scores and in the catalepsy induced by an acute haloperidol challenge with respect to saline treated rats. The present results indicate that a chronic uridine treatment is able to potentiate the reduction of the striatal DA transmission induced by acute and chronic haloperidol treatment. This finding suggests the possibility to reduce the neuroleptic dose in the treatment of schizophrenia by combining neuroleptic and uridine treatments, thus making it possible to relieve some of the side effects of neuroleptic therapy.

 

methylphenidate, i must assume? and forgive my impatience, but just send Flex a PM asking why it is bad, tell him I sent you and he can thank me later. ;) ok nvm you can spare him the annoyance, although he would also be amused

long story short, it's nearly as bad as amphetamine

and not to be overly pedantic or a science Nazi, but it doesn't contain dopamine, it reduces dopamine uptake, thereby increasing synaptic levels.

Methylphenidate Administration to Adolescent Rats Determines Plastic Changes on Reward-Related Behavior and Striatal Gene Expression
Administration of methylphenidate (MPH, Ritalin®) to children with attention deficit hyperactivity disorder (ADHD) is an elective therapy, but raises concerns for public health, due to possible persistent neurobehavioral alterations. Wistar adolescent rats (30 to 46 day old) were administered MPH or saline (SAL) for 16 days, and tested for reward-related and motivational-choice behaviors. When tested in adulthood in a drug-free state, MPH-pretreated animals showed increased choice flexibility and economical efficiency, as well as a dissociation between dampened place conditioning and more marked locomotor sensitization induced by cocaine, compared to SAL-pretreated controls. The striatal complex, a core component of the natural reward system, was collected both at the end of the MPH treatment and in adulthood. Genome-wide expression profiling, followed by RT-PCR validation on independent samples, showed that three members of the postsynaptic-density family and five neurotransmitter receptors were upregulated in the adolescent striatum after subchronic MPH administration. Interestingly, only genes for the kainate 2 subunit of ionotropic glutamate receptor (Grik2, also known as KA2) and the 5-hydroxytryptamine (serotonin) receptor 7 (Htr7) (but not GABAA subunits and adrenergic receptor alpha1b) were still upregulated in adulthood. cAMP responsive element-binding protein and Homer 1a transcripts were modulated only as a long-term effect. In summary, our data indicate short-term changes in neural plasticity, suggested by modulation of expression of key genes, and functional changes in striatal circuits. These modifications might in turn trigger enduring changes responsible for the adult neurobehavioral profile, that is, altered processing of incentive values and a modified flexibility/habit balance.

 

Methylphenidate (Ritalin) induces Homer 1a and zif 268 expression in specific corticostriatal circuits.
Corticostriatal circuits participate in limbic, attentional, motor and other networks, and are implicated in psychostimulant addiction. The psychostimulant methylphenidate is used in the treatment of attention-deficit hyperactivity disorder and for recreational purposes. Recent studies indicate that methylphenidate alters gene expression in striatal neurons. We investigated whether methylphenidate affects gene regulation in specific corticostriatal circuits, by comparing drug-induced molecular changes in different functional domains of the striatum with changes in their cortical input regions. In order to assess the potential functional significance of methylphenidate-induced molecular changes, we examined members of two different classes of plasticity-related molecules, the transcription factor zif 268 and the synaptic plasticity factor Homer 1a. Acute methylphenidate administration in adult rats increased the expression of Homer 1a and zif 268 in both cortex and striatum in a dose-dependent and regionally selective manner. These changes in gene expression occurred after doses of 2 mg/kg (i.p.) and higher, and were highly correlated between cortical regions and their striatal targets. In the cortex, increases were maximal in the medial agranular (premotor) and cingulate cortex, followed by motor and somatosensory cortex, and were minimal in the insular cortex. Correspondingly, in the striatum, increases were most robust in sensorimotor sectors that receive medial agranular input, and were weaker or absent in ventral sectors. The methylphenidate-induced increases in cortical Homer 1a and zif 268 expression were also correlated with increases in striatal substance P and dynorphin expression (direct pathway). Overall, the regional distribution of methylphenidate-induced molecular changes in the striatum was similar to that of changes induced by psychostimulants such as cocaine. These findings demonstrate that methylphenidate affects transcription and synaptic plasticity regulatory proteins in specific corticostriatal circuits, including those implicated in attentional functions and psychostimulant addiction. Such methylphenidate-induced gene regulation may contribute to the therapeutic effects and/or abuse liability of this psychostimulant.

 

Prefrontal cortical and striatal transcriptional responses to the reinforcing effect of repeated methylphenidate treatment in the spontaneously hypertensive rat, animal model of attention-deficit/hyperactivity disorder (ADHD)
Background
Methylphenidate is the most commonly used stimulant drug for the treatment of attention-deficit/hyperactivity disorder (ADHD). Research has found that methylphenidate is a “reinforcer” and that individuals with ADHD also abuse this medication. Nevertheless, the molecular consequences of long-term recreational methylphenidate use or abuse in individuals with ADHD are not yet fully known.
Methods
Spontaneously hypertensive rats (SHR), the most validated and widely used ADHD animal model, were pretreated with methylphenidate (5 mg/kg, i.p.) during their adolescence (post-natal day [PND] 42–48) and tested for subsequent methylphenidate-induced conditioned place preference (CPP) and self-administration. Thereafter, the differentially expressed genes in the prefrontal cortex (PFC) and striatum of representative methylphenidate-treated SHRs, which showed CPP to and self-administration of methylphenidate, were analyzed.
Results
Genome-wide transcriptome profiling analyses revealed 30 differentially expressed genes in the PFC, which include transcripts involved in apoptosis (e.g. S100a9, Angptl4, Nfkbia), transcription (Cebpb, Per3), and neuronal plasticity (Homer1, Jam2, Asap1). In contrast, 306 genes were differentially expressed in the striatum and among them, 252  were downregulated. The main functional categories overrepresented among the downregulated genes include those involved in cell adhesion (e.g. Pcdh10, Ctbbd1, Itgb6), positive regulation of apoptosis (Perp, Taf1, Api5), (Notch3, Nsbp1, Sik1), mitochondrion organization (Prps18c, Letm1, Uqcrc2), and ubiquitin-mediated proteolysis (Nedd4, Usp27x, Ube2d2).
Conclusion
Together, these changes indicate methylphenidate-induced neurotoxicity, altered synaptic and neuronal plasticity, energy metabolism and ubiquitin-dependent protein degradation in the brains of methylphenidate-treated SHRs, which showed methylphenidate CPP and self-administration. In addition, these findings may also reflect cognitive impairment associated with chronic methylphenidate use as demonstrated in preclinical studies. Future studies are warranted to determine the clinical significance of the present findings with regard to long-term recreational methylphenidate use or abuse in individuals with ADHD.

 

A Study on the Effect of Methylphenidate on Creativity of Healthy Adults

(above study has yet to be completed, or rather they're taking their sweet time processing the data, my guess is a negative result)

Roughly an equal ratio of receptor to transmitter, neither hyperdopamine nor hypo, but a happy middle, or perfect harmony.  That's what nature intended: not for us to disrupt her homeostasis.


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#16 permhealing

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Posted 01 November 2015 - 04:17 AM

On uridine: the only two studies are the ones I listed, and they say opposite things (one says increased dopamine release, the other says decreased).  The question is who will you choose to believe?

 

Well, just found a third study (1989, found via the book in my first post) is the only other I could find... so basically it's two studies against one.  66.7% chance you are right, it increases receptors, deceases transmitter.

 

 

 

 

If uridine increases the number of receptor but decreases neurotransmitter numbers, then could I compensate that by taking MP at the same time as uridine?

 

 

 

 

 

 

 

Trust me the theanine is such a weak overmethylator, the EGCG is gonna dominate, and leave you balanced, perhaps undermethylated.

Green tea also inhibits acetylation and deacetylation.  Also: https://www.google.c...Phosphorylation

 

 

 

 

Do you think choline is a strong or weak methylator?

 

http://lpi.oregonsta...yl-group-source



#17 gamesguru

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Posted 01 November 2015 - 01:58 PM

Unless dealing with high dopamine issues, it's a fine idea.  But even so, I would substitute ginkgo[1], ginseng[1], [2], green tea[1], [2], [3], [4], [5] for MP.

 

It's only a cofactor along with methionine groups in promoting normal methylation, but even so, too much choline can cause overmethylation.  With adequete folate[1], seems the role of choline is reduced even further.  So it's more of a broad methylator of medium-low strength.  Still, better not to be deficient. [1], [2], [3], [4], [5]

 

nutrients-05-03481-g001.jpg


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#18 MattH

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Posted 27 June 2018 - 05:49 AM

Hello, I just wanted to suggest the possibility that you have/had it the wrong way, and in fact your Dopamine receptor count was decreased. Yes, it is said CPD and to some extent Uridine "regrow" receptors here or there, but this has to be seen in context. For one CPD is primarily an acetylcholine booster, which is sort of the antagonist to dopamine, perhaps more strongly than serotonine (which is more like a competitor). Then, Uridine, as I've read, doesn't promote Dopamine receptor growth at all: it encourages the "renewal", but by way of decreasing them in total and at a faster rate first! (This can be useful to support balance, or even try to repair damage, but it doesn't seem a direct path to increase.)

That means, those together could very well give your dopamine receptors a blow. At least I doubt it gave you "too much" dopamine.

Something else on Uridine I had to think of: it is a strong GABA agonist, which could decrease your NMDA efficacy. I personnally have found issues in that regard, and find GABA strongly overrated in general (often doesn't feel good or right). I would suggest taking Uridine (if one wants to) together with a bit of l-glutamine to balance this effect.

Edited by MattH, 27 June 2018 - 06:03 AM.






Also tagged with one or more of these keywords: cdp, uridine, tolerance, virus, influenza, dopamine, receptor density, sam-e

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