“A dopamine antagonist (antidopaminergic) is a type of drug which blocks dopamine receptors by receptor antagonism. Most antipsychotics are dopamine antagonists”
so clozapine etc are all dopamine antagonists, they reduce the level of dopamine in your brain
is that roughly right?
is clonazepam (klonopin) a GABA agonist, it increases the level of GABA?
It’s not that antagonists reduce levels of neurotransmitters per se, but they reduce effects of those neurotransmitters by blocking their respective receptors. That’s how i understand this. Antagonists block receptors.
@ Far_Cry0
Yes but you don’t have schizophrenia, you said you only take AP to sleep, I just wanted to friendly open your eyes, it’s absurd to take risperidone to sleep, by blocking your dopamine without a real reason you are renouncing to your emotions, your motivations to do things, your hormones, your life… Please don’t say these are negative symptoms, before Invega I had plenty of emotions, motivation and libido, I’m writing this post because the other day I saw you complaining, you said “life sucks” , of course it does, you are taking a potent AP just to sleep. Feel free to ignore me, I just wanted to help, because I know how difficult is to live under paliperidone/risperidone.
Who said that…!!! Do u know whats written on icd 10… there are many sub type of sz…!!! Mine is called sz simplex… which means absence of positive symptoms…!!!
I not only take rispredal for sleep … it also helps with depression and anxiety also lift up my mood…
What are ur intension against me… are u trying to prove me wrong… dont ever say i dont have sz…
I am well adjusted here… i am trying to be kind with u…!!! Be careful before writing ur veiws…peace…
You could try increasing your Seroquel and decreasing the Risperidone, if you just want it for insomnia. That way you won’t block the dopamine in your brain so much.
It also helps me in negative and cognitive symptoms… like with out medication my memory is terrible … when i take my rispredal i find my memory a little sharp… i mean it doesnt help me 100% … but i feel i have improved to 25%…
I don’t think you’re being very helpful now, @Hhih_Gyhgh. We all say things sometimes that we don’t really mean. Far_cry0 has sz and feels better because of the meds. That’s what matters. He has negative and cognitive symptoms and a real sz diagnosis.
Don’t worry, I will never try to help anybody again, I’m done with this forum, anyway life without dopamine is not life to me. Dopamine is life, goodbye.
The quickest way to learn how to cope with your illness is to recognize it for what it is.
It’s way deeper than a chemical issue. Neurotypicals love seeing it that way… because they either see people as calm and normal… or erratic and crazy. They frankly won’t go deeper than that… We suffer from having a memory that ties both together and keep each state confused.
It’s just an illness that manifests as an experience. That experience is certifiably not true to life. If you look at the population base that lives with psychosis you’ll find no prejudice adds up.
It’s a fear complex… and honestly I do see it as a cognitive parasite. It does what ever it can to keep your attention so it can maintain it’s own structure…
Why does it do that? Lord only knows it’s fools errand to try and sort out. It could indeed be him in the end anyway… mysterious ways and whatnot.
In the end it’s just an illness. Try to solve it like some puzzle just feeds it. It’s an involuntary challenge to have to sort out the puzzle just to live… but that’s all it is… an endless puzzle that transcends are comprehension.
The best approach is to see that puzzle and then know that your better off too just look away. In neurology it’s called pruning… synaptic connections are trimmed when they go without use over time. It’s the only way to reverse the rapid-onset neuroplastic changes that occur upon first break.
If I were to say there was a knack to the schizophrenic… is that the mental adaptability of the brain is meant for new environments. It’s like a calling… and it makes sense that some were actually advantaged in the past in having that manifest destiny inside… because preemptively satisfying it was what led to the development of the modern world.
Raised in one environment… bound to exist in another very different one… it’s mandatory… and if we don’t find it we start spinning in ourselves due to lacking so much insight and appropriate challenge.
I like psychosis… it’s an interesting thing to ponder…
One key difference I see regarding acknowledging psychosis… there is a focus on psychosis (bad) and then there are thoughts about psychosis. The latter entails a more objective perspective and stronger ground for find insight around the illness instead of entertaining psychosis and letting it eventually have its way with you.
its not even necessarily caused by dopamine problems per se, just like depression isnt necessarily a monoamine deficieny per se, it could be a case of underlying structural differences causing those imbalances that we dont quite understand yet. but decreasing dopamine does help with psychotic symptoms in most patients, while increasing it in other places can potentially help negative symptoms, though thats far from a guarantee.
also, benzos arent actually agonists of gaba! theyre properly called allosteric positive modulators. per wikipedia, they “induce an amplification of the effect of the primary ligand” rather than actual agonism.
antipsychotics vary, some having affinity for muscarinic receptors (causing anticholinergic effects) while others dont, some affect adrenergic receptors, some dont, plenty affect histamine but others dont, but the common thread among first gens is that their main mechanism that unites them is their dopamine antagonism. second gen are united by both dopamine antagonist AND seretonergic effects, which i believe is why they have a lower rate of eps but a higher rate of metabolic problems. truthfully, though abilify/rexulti/vraylar are usually just called second gen aps, they should really be called third gen–united by dopamine antagonism, seretonergic activity, AND partial dopamine agonism (hence why they can be rather stimulating). the much hyped lumateperone would also be classified as a third gen antipsychotic (ive only ever seen one paper refer to them as third gen but i always thought it made more sense than calling them second gen), but seems like due to its presynaptic dopamine agonism and potential for 5-ht2a (a serotonin receptor) blockade it has less side effects and better efficacy for negative symptom treatment, though im cautious about that because when second gens came out they all hyped up how they wouldnt cause eps…yet they still can, just at a lower rate. so, who knows, we’ll see once its on the market.
Has anyone had their anhedonia or avolition go away from a dopamine partial-agonist? My pdoc told me that other antipsychotics like Geodon and Latuda can help with negative symptoms, but I’ve been anhedonic and amotivated for the past 6 months and I can’t take it anymore.
