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Dr. Bob is Robert Hsiung, MD,
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Posted by CrAzYmEd on May 24, 2010, at 22:42:06
In reply to Re: Also, posted by CrAzYmEd on May 23, 2010, at 12:25:01
But you are right there is no way to know "the way to go" it really depends on the situation, for example look at this study. 5HT2A agonists may be of benefit for OCD patients.
"
17) Perani D, Garibotto V, Gorini A, Moresco RM, Henin M, Panzacchi A, Matarrese M, Carpinelli A, Bellodi L, Fazio F
In vivo PET study of 5HT(2A) serotonin and D(2) dopamine dysfunction in drug-naive obsessive-compulsive disorder.
Neuroimage. 2008 Apr 27;
There are several lines of evidence, the majority indirect, suggesting that changes in serotonergic or dopaminergic neurotransmission may contribute to the pathogenesis of obsessive-compulsive disorder (OCD). We evaluated the co-occurrence of serotonergic and dopaminergic dysfunctions in OCD subjects, all drug-naive, with no co-morbidity and homogeneous for symptoms. Each subject underwent two positron emission tomography (PET) scans to measure in vivo both serotonin (5-HT(2A)) and dopamine (D(2)) receptor distribution. For this, we used [(11)C]MDL and [(11)C]Raclopride, highly selective antagonists of 5-HT(2A) and D(2) receptors, respectively. The comparison with a control group was carried out using both voxel-wise (SPM2) and regions of interest (ROI) approaches. There was a significant reduction of 5-HT(2A) receptor availability in frontal polar, dorsolateral, and medial frontal cortex, as well as in parietal and temporal associative cortex of OCD patients. We also found a significant correlation between 5-HT(2A) receptor availability in orbitofrontal and dorsolateral frontal cortex and clinical severity, suggesting a specific role for serotonin in determining the OCD symptoms. There was also a significant reduction of [(11)C]Raclopride uptake in the whole striatum, particularly in the ventral portion, possibly reflecting endogenous dopaminergic hyperactivity. The co-existence of serotonergic and dopaminergic dysfunction in the same homogeneous group of drug-naive OCD patients provides in vivo evidence for the complex molecular mechanisms of OCD, and represents the basis for further studies on the effect of therapeutic agents with specific modulatory effects on these neurotransmission systems. [PubMed Citation] [Order full text from Infotrieve]"
My point is that 5HT2A antagonism seems to be considered as allways good on these forums, and D2 antagonism should be the way to go too, while i disagree with both, it depends on the situation, and i beleive that many cases the other way around is good, those options seem to be ignored, 5HT2A is allways deemed as "bad".
Posted by linkadge on May 24, 2010, at 22:42:07
In reply to Re: Let's Have Dopamine Pie For Lunch, posted by CrAzYmEd on May 23, 2010, at 17:03:03
Pretty much all dopamine agonists have a U shaped theraputic window for their theraputic effects.
Dopamine in the prefrontal cortex can enhance cognition, but (in the stress model that Brainbeard mentioned) a anxiogenic beta carboline was used which can greatly enhance dopamine neurotransmission. If it gets too high, there is cognative disturbance.
The same thing goes with dopamine in the NAC. If dopamine levels get too high, they can produce apathy and anhedonia just as if levels are too low.
I would say that the 5-ht2c antagonism has a greater effect on dopamine in the neucleus accumbens. The 5-ht2 receptors affect the prefrontal cortex more.
Linkadge
Posted by linkadge on May 24, 2010, at 22:42:07
In reply to Re: Let's Have Dopamine Pie For Lunch, posted by CrAzYmEd on May 23, 2010, at 17:06:40
I would use a low dose of a typical AP such as perphenazine if dopamine antagonism is desired. There is low risk of TD as well as diabets.
Linkadge
Posted by linkadge on May 24, 2010, at 22:42:07
In reply to Re: Also, posted by CrAzYmEd on May 23, 2010, at 17:42:05
Is this med a 5-ht2b agonist? LSD is. This is very bad for cardiac valves. This is why cabergoline was pulled.
Linkadge
Posted by Brainbeard on May 24, 2010, at 22:42:08
In reply to Lisuride And The Real Life, posted by Brainbeard on May 23, 2010, at 17:17:50
I found a lisuride experience of somebody who took it to induce hypersexuality here: http://www.asiatour.com/lisuride1.htm. It starts off with some interesting description of initial lisuride use, then wanders off into irrelevant musings. Don't bother with the second part, it hardly addresses lisuride at all anymore.
I also found a research abstract which illustrates my point that dopamine agonists are not dopamine boosters. It (http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6TBR-44PC749-13&_user=10&_coverDate=02/28/2002&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1345452728&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=1adc7e92e2efacbb18286e0a1442e749) says: ' This study supports the view that alcoholics may relapse due to decreased dopamine function, resulting from intake of dopamine D2 receptor agonists. In particular, our data do not support the use of lisuride for relapse prevention in alcoholics.'
There you have it. Lisuride and other D2-agonists may decrease dopamine function, at least in part.
On the other hand, lisuride yields EEG's similar to psychostimulants: http://www.erowid.org/references/refs_view.php?ID=3243
From a patent to use liusuride in alcoholism (http://www.freepatentsonline.com/4096266.html):
'Lisuride (.....) was synthesized by Zikan and Semonsky (Zikan, V., M. Semonsky: Coll. Czech. Chem. Commun. (1960), 1922) in order to develop an LSD-25 analog with antiserotonin and antihistamine properties without having hallucinogenic side effects. (.....)
In one of the first clinical trials, Vojtechovsky et al (Activ. Nerv. Super. 5 (1963), 211) found in about half of the cases a moderate inhibitive dysphoric effect, while in about one third they found a slight central nervous system (CNS) effect without autonomous symptoms. In half of the subjects, however, the changes were so slight that they could not be distinguished from placebo. Lisuride did not alter the mental functions in psychological tests. (.....)'
The article also points out that lisuride can be effective against migraines as well as neurasthenia.
Incredible potential? A 'moderate inhibitive dysphoric effect' or a 'slight central nervous system effect' doesn't sound all that fancy to me. As a standalone drug, I think lisuride has only limited use.
Posted by CrAzYmEd on May 24, 2010, at 22:42:08
In reply to Re: What about 5-ht2b? Bad for cardiac valves?, posted by linkadge on May 23, 2010, at 18:06:15
Linkadge, its a 5HT2B antagonist, it wont cause cardiovascular damage.
Lisuride, a dopamine receptor agonist with 5-HT2B receptor antagonist properties: absence of cardiac valvulopathy adverse drug reaction reports supports the concept of a crucial role for 5-HT2B receptor agonism in cardiac valvular fibrosis.
Hofmann C, Penner U, Dorow R, Pertz HH, Jähnichen S, Horowski R, Latté KP, Palla D, Schurad B.Global Medical Safety, Schering AG, Berlin, Germany. [email]christoph.hofmann@schering.de[/email]
Abstract
OBJECTIVES: The high incidence of fibrotic cardiac valvulopathies reported in association with the 8beta-ergoline dopamine (DA) agonist, pergolide, and also case reports for cabergoline and bromocriptine have made it necessary to review the theoretical basis and actual findings in the case of another DA agonist, the 8alpha-ergoline lisuride (used since the 1970s for migraine prophylaxis as well as since the 1980s for its prolactin-lowering and anti-Parkinson activity). METHODS: We have reviewed the pharmacology of lisuride in relation to other DA agonists, and we have performed a throughout literature search as well as a search of our own and other adverse drug reaction databases for a possible relationship of lisuride with cardiac valvulopathy or for any reports of fibrosis in other locations. RESULTS: Our review of the pharmacology and the literature strongly suggests that drug-induced cardiac valvulopathies are always related to a stimulatory drug effect on trophic 5-HT(2B) receptors. As lisuride is devoid of such an effect, but on the contrary is an extremely potent 5-HT(2B) antagonist, an association of lisuride therapy with cardiac valvulopathies seems to be highly unlikely. In agreement with this hypothesis, not a single report of a cardiac valvulopathy associated with lisuride therapy has been identified in any database so far.Furthermore, against a background of an estimated 360,000 patient years, we have found only a very small number of cases of any other form of fibrosis (1x retroperitoneal, 2x pleural, 2x pulmonary, 1x interstitial pulmonary changes), in part combined with other risk factors and confounding variables. This closely matches 4 reports available from WHO (1x retroperitoneal, 3x pleural fibrosis). In addition, only 5 other possibly related conditions (3x pleural effusion, 1x pleuritis, 1x pericarditis) were identified in the lisuride adverse drug reaction database of Schering, Berlin. CONCLUSIONS: No link has been found between lisuride use and fibrotic cardiac valvulopathy, in agreement with the 5-HT(2B) receptor antagonist effect of this drug. The very low incidence of spontaneous reports of any other fibrosis could be even compatible with an association by chance in the population exposed to lisuride. Although close monitoring for this kind of side effects is still to be recommended in the therapy with lisuride, our data do not support the concept of a class effect suggesting that all ergot-derived drugs and especially DA receptor agonists with some chemical similarity to the ergot structure will cause or facilitate cardiac valvulopathies as observed with pergolide.
Posted by CrAzYmEd on May 24, 2010, at 22:42:08
In reply to Lisuride Experiences: Mixed Bag, Not The New Cool, posted by Brainbeard on May 23, 2010, at 18:13:42
brainbeard: Those studies where they described a moderate effect, was lisuride used for several weeks or acutely? Negative effects can be expected the first weeks due to a decrease in dopaminergic transmission.
(Yeah i know dopamine agonists decrease dopamine at first, but this completely recovers after a while, leaving you with the originial dopamine transmission the dopamine agonism."After 14 days of PPX treatment, the firing rate of DA had recovered as well as that of NE, whereas the firing rate of 5-HT neurons was increased by 38%. It was also observed that sustained PPX administration produced desensitization of D(2)/D(3) and 5-HT(1A) cell body autoreceptors, as well as a decrease in sensitivity of alpha(2)-adrenergic cell body autoreceptors. These adaptive changes are implicated in long-term firing rate adaptations of DA, NE and 5-HT neurons after prolonged PPX administration. In conclusion, the therapeutic action of PPX in depression might be attributed to increased DA and 5-HT neurotransmission."
Posted by CrAzYmEd on May 24, 2010, at 22:42:09
In reply to Re: Lisuride Experiences: Mixed Bag, Not The New Cool, posted by CrAzYmEd on May 23, 2010, at 18:19:43
This study found lisuride effective for 80% of the patients, but then again this wasnt for regular depression but depression after a stroke.
[Therapeutic effect of lisuride maleate on post-stroke depression]
[Article in Japanese]Hougaku H, Matsumoto M, Hata R, Handa N, Imaizumi M, Sugitani Y, Yoneda S, Etani H, Sueyoshi K, Kusunoki M, et al.
First Department of Medicine, Osaka University Medical School.
Abstract
Twenty post-stroke depressive patients who obtained more than 11 points on Self-Rating Questionnaire for Depression, were treated with 0.075 mg/day lisuride maleate for 12 weeks. The drug effect on depression was evaluated quantitatively by the Hamilton Rating Scale for Depression. The relationships between brain CT or MRI and SRQ-D score were investigated in 24 subjects. More than 80% of post-stroke depressive patients improved after lisuride maleate treatment for 8 or 12 weeks. In particular, depressed mood, hypobulia, sleep disturbance, anxiety, etc. were significantly improved compared to the baseline condition. As for the relationships with CT and/or MRI findings, the group with moderate to severe brain atrophy had a significantly higher grade of depressive state than those without.
Posted by linkadge on May 24, 2010, at 22:42:10
In reply to Lisuride Experiences: Mixed Bag, Not The New Cool, posted by Brainbeard on May 23, 2010, at 18:13:42
I don't buy the notion that dopamine agonists decrease dopamine function (overall). If this were true, why are they effective (long term) for parkinsons disase?
Some agonists, like mirapex, have preferential effects on the presynaptic dopamine receptor. Over time, the drug might well downregulate the dopamine autoreceptor and thus enhance neurotransmission.
Linkadge
Posted by Brainbeard on May 24, 2010, at 22:43:11
In reply to , posted by on December 31, 1969, at 18:00:00
> I don't buy the notion that dopamine agonists decrease dopamine function (overall). If this were true, why are they effective (long term) for parkinsons disase?
You can only expect them to, since they mimick dopamine, binding to dopamine receptors, pushing the real thing out of the way. This is supposedly the reason why non-ergoline dopamine agonists cause sleep attacks.
I believe that OCD is a form of hyperdopaminergic activity, and that SSRI's work for OCD because of their anti-dopaminergic properties. But the overall story is so complex, I readily admit that I only understand a tiny bit of the whole picture.
Posted by CrAzYmEd on May 24, 2010, at 22:44:00
In reply to , posted by on December 31, 1969, at 18:00:00
Personally i beleive that the low dopamine binding in OCD comes from hyperactive glutamate activity (just as glutamate hyperactivity seems to cause low dopamine binding in ALS).
--------------------------------------
Decreased striatal dopamine-receptor binding in sporadic ALS: Glutamate hyperactivity?O. J. M. Vogels, MD, PhD, W. J. G. Oyen, MD, PhD, B. G. M. van Engelen, MD, PhD, G. W. A. M. Padberg, MD, PhD and M. W. I. M. Horstink, MD, PhD
From the Departments of Neurology (Drs. Vogels, van Engelen, Padberg, and Horstink) and Nuclear Medicine (Dr. Oyen), University Hospital Nijmegen, the Netherlands.Address correspondence and reprint requests to Dr. O.J.M. Vogels, Department of Neurology, University Hospital Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, the Netherlands.
The pathogenesis of ALS may be related to increased glutamatergic excitotoxicity. The striatum receives massive glutamatergic input. Animal studies suggest that glutamate decreases striatal D2-receptor synthesis. In drug-naïve, sporadic ALS patients we demonstrated decreased striatal D2-receptor binding in vivo that could be partially reversed by the glutamatergic transmission blocker riluzole. Our findings support the glutamatergic excitotoxicity hypothesis in sporadic ALS.
--------------------------------------------Memantine has been shown effective for OCD (it did wonders for wine) while it hasnt got any anti dopaminergic activity, instead it can upregulates dopamine receptors (altough no idea how significant this is in therapeutic relevant doses) and has dopamine agonist properties itself.
But yeah its really complex, and this is my own little theory :p, but i dont buy the too much dopamine theory.
Interesting discussion besides:p.
Posted by CrAzYmEd on May 24, 2010, at 22:44:00
In reply to Lisuride, incredible potential, posted by CrAzYmEd on May 23, 2010, at 7:18:25
Srry if i sound like a found a new miracle, i'm just interested in lisuride and think it can be a interesting med.
Posted by Brainbeard on May 24, 2010, at 22:44:00
In reply to Not wonder med, just interested in it., posted by CrAzYmEd on May 24, 2010, at 6:11:45
Interesting discussion indeed. Wouldn't have been possible had we agreed. ;)
You got me interested in lisuride too, I just don't feel attracted to the initial nausea it is likely to produce.
On the other hand, how cool it would be to be on a chemical sister of LSD?!
And reducing prolactin levels seems like a good idea when on antidepressants and antipsychotics that can cause hyperprolactinemia, like myself.
Posted by CrAzYmEd on May 24, 2010, at 22:44:00
In reply to Disagreeing, The Holy Grail And Man-Boobs, posted by Brainbeard on May 24, 2010, at 10:50:08
I wonder how this one would work with amisulpiride or sulpiride. With the combination we wouldnt have to wait for the autoreceptors to downregulate as it would keep the lisuride off the autoreceptors so it can go directly to the postsynaptics. (A friend of me has good succes with the sulpiride/pramipexole combo).
Also maybe the amisulpiride would block some of lisuride's agonism in the puking center, while lisuride blocks the huge prolacting increase by amisulpiride.
This would only work if ami's affinities for the presynaptic receptors is higher then lisuride, so lisuride doesnt knock it off the autoreceptors. But it appears to work with pramipexdole.
Just an idea.
I will try to get ahold of lisuride myself, would be awesome if i found a open minded doc so it would be insured by the goverment:p.
Besides, props to you man, ive seen some of your old posts, very good information and contributions you post here.
Posted by Brainbeard on May 24, 2010, at 22:44:43
In reply to , posted by on December 31, 1969, at 18:00:00
Posted by Brainbeard on May 25, 2010, at 15:45:51
In reply to Lisuride, incredible potential, posted by CrAzYmEd on May 24, 2010, at 22:41:53
http://www.freepatentsonline.com/4045562.html:
'Lisuride and the physiologically acceptable salts thereof are psychic energizers without simultaneously exhibiting the disadvantages (stimulating effect and development of dependency) of the phenylethylamine derivatives. There is a significant therapeutic effect in so-called neurasthenic symptomatology, mainly in the following symptoms: loss of interest, loss of drive and activity, loss of energy and functional capacity, loss of concentration and learning ability. They possess surprisingly high compatibility even at the large doses of this invention and there is no development of dependency, even after long-term administration at these large dosages.
The spectrum of psychic energizer activity, discovered with the aid of the quantitative Pharmaco-EEG, (T. M. Itil; Diseases of the Nervous System 8 (1972) 8) is novel and has not been found for another drug. The objective results are laid down in parameters of the EEG's analyzed by computer and the spectrum of effectiveness is characterized by a decrease of the delta and theta waves, and increase in the alpha and slow beta waves, as well as a decrease of the superimposed fast waves (up to 100/second). These phenomena affecting the physiology of the brain point to certain stimulating and simultaneously inhibiting effects exerted by lisuride. Accordingly, lisuride has a clinical spectrum of activity which can be called "Energizer Anxiolytic" (T. M. Itil et al., Int. J. Clin. Pharmacol. Ther. & Toxicol. 10[ 1974] 143).'
Posted by CrAzYmEd on May 25, 2010, at 17:04:05
In reply to Lisuride, The Anxiolytic Energizer?, posted by Brainbeard on May 25, 2010, at 15:45:51
That is really interesting! Good find.
Posted by Brainbeard on May 26, 2010, at 5:55:33
In reply to Re: Lisuride, The Anxiolytic Energizer?, posted by CrAzYmEd on May 25, 2010, at 17:04:05
A pity this stuff has such a short half-life. That'll make titration even more difficult.
Posted by CrAzYmEd on May 26, 2010, at 6:50:24
In reply to Re: Lisuride, The Anxiolytic Energizer?, posted by Brainbeard on May 26, 2010, at 5:55:33
But its possible to make a time released preparation. I forgot how to do it again tough, will try to find it.
Posted by Conundrum on May 27, 2010, at 21:02:04
In reply to Let's Have Dopamine Pie For Lunch, posted by Brainbeard on May 24, 2010, at 22:42:05
If you do some searching around the web you can find that 5 HT2A agonism by LSD promotes learning in rats and 5 HT2A antagonism deters learning. Maybe not in humans though. I think in humans its more trouble than its worth. Seems to cause sexual side effects and what fun is that?
Posted by Conundrum on May 27, 2010, at 21:18:00
In reply to Re: Let's Have Dopamine Pie For Lunch, posted by linkadge on May 24, 2010, at 22:42:07
I didn't know that. I guess anything is possible. How would one know if they're anhedonia is caused by too little or too much dopamine. Is there any differentiation in other symptoms.
I've tried some dopaminergic supplements and drugs like wellbutrin and ritalin which never did anything for me. Also before the anhedonia got worse I did have some paranoia like listening to conspiracy theorists and into spirituality, which is now gone but I can think more logically. Interestingly these feelings of spirituality and interconnectedness of all things started after stopping prozac, so it seems like a dopaminergic rebound. Then after taking ginkgo for two years and stopping all these feelings disappeared good and bad.
I feel as if my dopamine or noradrenaline dropped, but is it possible it went too high? I am being treated for slightly elevated blood pressure, but that might just be because I'm slightly overweight. I guess the only way to find out would be to try an antipsychotic med. I'm still leaning towards low catecholamines though.
Posted by CrAzYmEd on May 28, 2010, at 6:14:47
In reply to Re: Let's Have Dopamine Pie For Lunch » Brainbeard, posted by Conundrum on May 27, 2010, at 21:02:04
What causes sexual side effects? Lisuride will have PRO sexual effects like all other dopamine agonists by lowering prolactin.
Yes, LSD can increase learning but it does alot more then just 5HT2A agonism (its binding is very simular to lisuride).
LSD: 4.00 5ht1b, 3.77 5ht7, 3.75 5ht6, 3.73 5ht1a, 3.70 5ht1d, 3.64 5ht5a, 3.54 5ht2a, 3.16 D3, 3.11 5ht2b, 3.11 5ht2c, 2.93 Alpha2A, 2.62 5ht1e, 2.55 D2, 2.39 D4, 2.34 D1, 2.05 D5, 1.54 Alpha1A, 1.40 H1, 1.39 Beta1, 1.05 Beta2, 0.65 Alpha1B; 0.00: KOR, DOR, DAT, SERT, MOR, NET; ND: Sigma2, Alpha2B, Alpha2C, Imidazoline1, M1, M2, M3, M4, M5, Sigma1, H2, CB2, CB1, Ca+Channel, NMDA
(4 is best affinity, and under 2 not significant).
Posted by CrAzYmEd on May 28, 2010, at 6:18:27
In reply to Too much dopamine causes anhedonia? » linkadge, posted by Conundrum on May 27, 2010, at 21:18:00
Prozac wont cause a dopamine rebound as it raises dopamine itself: (It can really be anything, its impossible to point a effect of the withdrawal to any receptor)
---------------------------------
http://www.ncbi.nlm.nih.gov/pubmed/15741747
"Twelve patients affected by major depression received a single oral dose of fluoxetine in the morning, 5 mg in the first 5 days, 10 mg from the 6th to the 10th day and 20 mg from the 11th to the 40th day. Twelve healthy subjects received a placebo under identical testing procedures. Blood samples were collected at baseline and 7, 10 and 24 h after drug administration on the 1st day of fluoxetine administration at a dose of 5 mg, and on the 1st and the 30th day of fluoxetine administration at a dose of 20 mg (days 11 and 40 of treatment, respectively). We found that plasma norepinephrine, epinephrine and dopamine levels significantly increased after acute and chronic treatment (p < 0.001), reaching the highest concentrations on the last day. No significant changes of these parameters were observed in control patients."
-------------------------------------
I highly suggest against antipyschotics for the treatment of anxiety or depression, they should only be used to treat psychotic disorders. The risk of tardive dyskinesia and metabolic problems are not wort it.
Posted by Conundrum on May 28, 2010, at 9:23:31
In reply to Re: Too much dopamine causes anhedonia?, posted by CrAzYmEd on May 28, 2010, at 6:18:27
I think that prozac would still have a suppressive effect on dopamine in some areas of the brain though. I believe this is why it is effective in the treatment of OCD.
Interestingly the first 2 years off prozac my memory was bad so I took ginkgo for those first two years. It had a very powerful effect on me and if I took to much I had much more physical endurance and couldn't sleep. Like too much oxygen. Anyway a month after stopping it all the spiritual and loving feelings went away and I was hit with even worse anhedonia. At least then I was able to rid myself of those things. I was never into astrology or numerology before that or believed in conspiracies. I became better at using the logical part of my mind and eliminating unhelpful believes. So I guess in a way its has been helpful. I have no idea the physiology behind any of that though.
I have a similar feeling about atypical APs but it seems like psychiatrists are more comfortable prescribing them than tricyclics!
Posted by CrAzYmEd on May 28, 2010, at 9:47:04
In reply to Re: Too much dopamine causes anhedonia? » CrAzYmEd, posted by Conundrum on May 28, 2010, at 9:23:31
I dont buy the high dopamine OCD theory, this theory only comes from the low D2 bindin in humans and the fact that antipsychotics work for it.
However, there is loads of evidence for glutamate hyperactivity in OCD, glutamate downregulates D2, wich could be the cause of low D2 binding.
Also a good friend of me had moderate succes with pramipexole for OCD (and this isnt due to reduced dopamine, as he's autoreceptors are fully downregulated by now).
While i havent tried a dopamine agonist, i know that drugs that increase dopamine and NMDA antagonists are highly effective for my OCD.
Memantine, is a D2 agonist besides its nmda antagonism and has been found effective for OCD, prozac wich increases dopamine has been found effective for OCD too.
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