Hmm I don't think it's possible to up-regulate dopamine receptors 24/7. Unless we can find a way to avoid homeostasis. So dopamine agonists probably won't work but CrazyMed has hopes in lisuride so maybe that one will work but I still have my doubts. So what's left? Anti depressants that inhibits and/or release dopamine and the common stimulants.maybe we should find some way to upregulte dopamine receptors without direct use of dopaminergics instead of using dopamine agonists.
If they have a bad withdrawal doesnt mean they dont work, both ehsan and guide4dummies didnt report a decline in effectiveness.So dopamine agonists probably won't work
lol, blunted hedonia is marks saying of anhedonia (hedonia being the opposite of anhedonia).Wow, that's pretty cool you were using a dopamine agonist! I would like to try that sometime, though not for SA, for fun! And yeah, withdrawl would definitely be expected, as your dopamine recoptors have deregulaed...dopamine defencency.
Luckly the brain is an amazing organ and you will eventually feel better. I wonder if opiates would help the withdrawls any?
BTW what is hedonia??
I was thinking about taking them while on cocaine!lol, blunted hedonia is marks saying of anhedonia (hedonia being the opposite of anhedonia).
Dopamine agonists for fun? do you mean to have sex on? As they wont be much fun on their own, pramipexole would cause anxiety and anhedonia.
one month.How long were you on this combo and how long did the withdrawal syndrome last?
i don't like meds that stop working or worsen the problem after discontinuation. in my case using dopamine agonists worsened SAD after discontinuation and it isn't weird.If they have a bad withdrawal doesnt mean they dont work, both ehsan and guide4dummies didnt report a decline in effectiveness.
If i plan to stay on a med forever i dont mind it having a bad withdrawal.
It could (if withdrawal is because of reduced D2 density and glutamate hyperactivity), mark wasnt on memantine the last few weeks and when he was he underdosed (he was only on it for a short time tough).I thought that the use of memantine also prevented from withdrawal symptoms ... I was too confident
I think NMDA antagonists are the most effective option to upregulate dopamine receptors, maybe try a differend one then memantine as you didnt like it?one month.
withdrawal syndrome including depression,anxiety,headache, lack of energy and fatigue persisted for about 1 month. however i still feel my SAD is worse than before its use.
i don't like meds that stop working or worsen the problem after discontinuation. in my case using dopamine agonists worsened SAD after discontinuation and it isn't weird.
anyway, stratial dopamine binding affinity is lower than normal in SAD(maybe a genetic problem) and it seems using dopamine agonists and releasers are the only effective ways now.
i read somewhere that froskolin upregulates dopamine d2 receptors in striatum of RATs but i don't know if it is of clinical significance or not.
This doesnt appear to be the case, as anecdotally tolerance to dopaminergic drugs seems recovers faster with memantine then without. NMDA antagonism upregulates D2 but doesnt downregulate it, a hyperactive glutamine system downregulates it. Memantine doesnt freeze homeostasis, it just that nmda antagonism has a positive effect on the binding of several receptors.i disagree.
i think memantine should have a negative role here which is ignored.
maybe memantine inhibits rapid change in dopamine receptors' count after discontinuation of dopamine agonist(upregulation) through NMDA blockade.
memantine has a very long half-life(80-100hours) and will remain in blood for a very long time.
this can delay the recovery of dopaminergic system.
in fact, memantine will decelerate downregulation of dopamine receptors but also decelerate the process of upregulation(recovery).
Memantine to the rescue?Memantine attenuates the increase in striatal preproenkephalin mRNA expression and development of haloperidol-induced persistent oral dyskinesias in rats
Ole A. Andreassena, , , Jo Waageb, Bente Finsenc and Hugo A. Jørgensenb
a The Research Section, Department of Psychiatry, University of Oslo and Ullevål University Hospital, Kirkeveien 166, 0407, Oslo, Norway
b Department of Psychiatry and Locus on Neuroscience, University of Bergen and Bergen Psychiatric University Hospital, Bergen, Norway
c Department of Anatomy and Neurobiology, Institute of Medical Biology, University of Southern Denmark, Odense, Denmark
Accepted 16 September 2003. ; Available online 6 November 2003.
Tardive dyskinesia (TD) is a serious motor side effect of long-term neuroleptic treatment that may persist after drug withdrawal. Alterations in striatal enkephalinergic neurons due to excessive glutamatergic activity is a possible pathogenetic mechanism. We studied the effect of the NMDA antagonist memantine in a rat model of TD, in which vacuous chewing movements (VCM) were induced by 20 weeks of haloperidol administration. The striatal density of preproenkephalin mRNA was measured and the number of neurons estimated. Haloperidol induced persistent VCM that was associated with increased striatal expression of preproenkephalin mRNA. Memantine inhibited the development of haloperidol-induced persistent VCM and attenuated the increase in preproenkephalin mRNA expression. This suggests that glutamate-mediated up-regulation of striatal enkephalin plays a role in the development of haloperidol-induced persistent oral dyskinesias.
Do you think it's OK to take Mirapex recreationally for a libido boost? Maybe a handful of times per year?My severe withdrawal case is very rare. You would probably get 2-weeks tops. It may get very tolerable after only 1 week.
My withdrawal lasted for 5 months and I had to take other medications to become better. Now it's 95% over and I'm still getting better, which I'm very thankful for.