Treatments for anhedoniaViewing 6 posts - 1 through 6 (of 6 total)
Viewing 6 posts - 1 through 6 (of 6 total)
February 24, 2015 at 6:39 am #39876
InSaNe_BBMemberMay 13, 2015 at 10:04 am #373248
my current stack is 10mg dexedrine spansule, 21mg nicotine patch and 1mg clonazepam after trying hundreds of drugs this makes me feel most normal in regards to social anxiety and anhedonia. i really think d2 receptor availability in the striatum due to the a1 allele and abnormal gaba binding in certain brain areas are the primary causes, glutamate release being a secondary cascade effect similar to cAMP.May 13, 2015 at 10:04 am #373276
[QUOTE=socialpiranha;667835]my current stack is 10mg dexedrine spansule, 21mg nicotine patch and 1mg clonazepam after trying hundreds of drugs this makes me feel most normal in regards to social anxiety and anhedonia. i really think d2 receptor availability in the striatum due to the a1 allele and abnormal gaba binding in certain brain areas are the primary causes, glutamate release being a secondary cascade effect similar to cAMP.[/QUOTE]
Hmm. Doesn’t memantine upregulate D2 in the striatum? I’ve always had reasonable anhedonia and memantine didn’t help me at all. It gives me a psychotic type of reaction.
How long have you been on dexedrine? Does potential tolerance issues concern you?May 13, 2015 at 10:04 am #373277
[QUOTE=rjm07;667868]Hmm. Doesn’t memantine upregulate D2 in the striatum? I’ve always had reasonable anhedonia and memantine didn’t help me at all. It gives me a psychotic type of reaction.
How long have you been on dexedrine? Does potential tolerance issues concern you?[/QUOTE]
nope memantine is an agonist at the d2 receptor though similar to pramipexole but neither have any effect on receptor upregulation or density in the striatum afaik. pramipexole gives me a psychotic nauseated “strange’ feeling too i believe this is because its not about filling those receptors at all times as much as it is having enough receptors available so that when endogenous dopamine is supposed to enter them it can. they are not meant to be filled all the time only when a reward is needed to facilitate action.
when there is a deficit of d2 receptors and they are constantly filled, the brain is in conflict because one signal is saying we need to fill more d2 receptors because the reward is not enough to facilitate this action, while another is saying but all the d2 receptors are filled so this creates a catch 22 which is that “i need something but i dont know what it is” feeling to which the body responds by releasing more dopamine only to find other d receptors to fill exacerbating the problem. when this doesnt work the endocannibinoid system is employed to modulate calcium signalling in order to find a creative solution to the lack of reward object/stimulus. because of this lack, attempts/ideas get more imaginative “less confined to the norm” and less rational as they branch outward seeking for a rewarding stimulus. sometimes these extremely rewarding objects/experiences are found but more often nothing is found and dynorphin is released and adrenaline release is suppressed in defeat in order to immobilize the subject until a later more opportune time.
This would explain the back and forth between and overlap of (hypersexuality, heightened energy, disregard of consequence, risk taking/gambling, rapid, disorganised or irrational thinking, substance abuse and overall novelty seeking)
(depression, fatigue, irritability, hopelessness, lack of motivation, social isolation and immobilization ) in schizophrenia, bipolar, adhd, and dopamine agonist use and other psychiatric disorders.
other dopaminergics have this effect as well but its extent depends on their mechanism of action dosage individuals genetics/current biochemical status etc. marijuana can also have this effect due to its direct effect on the cannibinoid system although dosage and individuals genetics/current biochemical status are factors here as well. i suspect many other drugs can have this effect as well but this is probably all just bullshit anyway
a couple years ago i took dexedrine everyday for over a year and only had tolerance to the anxiolytic effect it had. motivation and concentration were uneffected at a stable dose. i have a feeling the gaba a agonism will prevent any loss of effectiveness but its only been a week lol so what do i know.
that being said i am concerned about tolerance/depletion of catecholamine stores etc but unfortunately i dont react well to nmda antagonists. i will be experimenting with verapamil in place of the clonazepam within the week tho as ive read calcium channel blockers also reduce tolerance. possibly some experimenting with methylene blue and candesartan as well as i have had responses to them in the past.
verapamil is my focus right now though as it has also shown the ability to alleviate both hypomania and depression. I believe excessive glutamate release and subsequent (excitotoxic) damage (as well as depletion of neurotransmitter stores) is the cause of tolerance to amps effects which might explain why nmda antagonists and calcium channel blockers and possibly gaba agonists have shown efficacy.
I think a lot of people see studies saying nmda antagonists block reverse tolerance(meaning maintains side effects) and interpret it as nmda ants reverse amphetamine tolerance. I havent seen any evidence that nmda antagonists reverse or reduce tolerance to the effects while leaving efficacy intact. all the evidence i have seen for the reasoning behind it is that nmda ants block ion channels preventing calcium from entering. so if all its doing is preventing calcium influx(therefore decreasing glutamate release therefore excitotoxicity and subsequently tolerance) then why not just take a calcium channel blocker and not screw up your d2 receptor binding with memantine if calcium really is the culprit. unfortunately i have a feeling exitotoxicity is inevitable with euphoric doses of stimulants but hopefully im wrong.May 13, 2015 at 10:20 am #373863
[QUOTE=hawior;666798]For me the best stuff is gbl, which improve glutamate.[/QUOTE]
Amisulpride increases glutamte release, too, just like GHB/GBL. It also stimulates the GHB receptor, allbeit, in a more theraputic manner (for day to day use, anyway) than GHB/GBL.
Have you ever ever considered that as a more sensible option?May 13, 2015 at 10:21 am #373896
For me the best stuff is gbl, which improve glutamate.
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