A-thing.txt

gistfile1.txt

it's y sarcosine (a glycine transporter inhibitor which increases glutamate transmission & modulates it as well) has been well-proven in research 2 decrease negative symptoms of schizophrenia AKA the perceptual hallucinations, emotional flatness, depression & demotivation etc. Then 4 example, a dopamine D2 antagonist will knock ur ass out & make u lethargic, demotivated, depressed, & seemingly numb or "empty", almost even. It's y benzos & opiates both can ac2ly help p profoundly as acute "silencers" so 2 speak of intense delusionally manic, or just generally intense psychotic episodes. w/ or w/o hallucinations, but beznos when taken acutely during a psychotic episode, even w/o concurrent antipsychotic administration (tho it most often is, & DEF should be unless theres drug allergies or contraindctions which would be p rare), but even sole benzo administration has shown 2 reduce hallucinations. As an analogy but technically not rly an actual neurochemical similiarty, its HYPERBOLICALLY kinda like taking a benzo as a trip killer during an acid trip. But again, it's not the same thing bc psychs besides maybe some bad headspaces im certain circumstances, can be compared 2 actual psychosis as i've exp it a couple times bc of my BPD which manifests during manic highs & lows v rarely as psychotic symptoms, too. anything that slows & shuts the brain up as a whole, will make all ur shit v simplified slow down, including the dysfucntional pts. but the psychosis from dopaminergics r most often related 2 either the obv predisposition or pre-existing mental disorder much like psychs, or lack of sleep/nutrition/hydration. or combo w/ other drugs w/ a propensity 2 envoke "drug-induced psychosis" its y they use PCP in basically evry animal study model when tryna replicate schizophrenia. it both blocks the action of glutamate unselectively, & increases the action of stimulatory catecholamines. so increased dopamine, v low glutamatergic transmission. u give some1 on PCP a D2 antagonist antipsychotic? the manic thoughts r entirely gone, & what happens is now the patient is now much closer 2 essentially being in that pre-khole headspace. if NMDA antagonism is reversed either fully or partially, the khole-like headspace & ESP the hallucinations, dissapate entirely. bc theres lots of ppl who will take shitloads of meth which release inconceivably and unaturally high lvls of catecholamines all @ once extensively, but never go psychotic until the sleep deprivation kicks in. but every single person that takes NMDA antagonists like ketamine, PCP, or dxm, begin 2 hallucinate. in a high enoguh dose of meth, youll go crazy bc of hyperactivity panic, & such an inflated sense of self u lose touch w/ anything else. but again, w/o other confoudning factors such as sleep deprivation, huner, dehydration, or lack of sleep, hallucinations from sole dopamine release isnt rly common @ all. tho profound neurotoxicity could also fairly be a cause in some rare cases, akin 2 MDMA/MDA's partial cause 4 those dph-esque hallucinations in high enough doses. & schizophrenia ISNT NMDA anntagonism I should add/clarify, its NMDAR HYPOFUNCTION. so except in rly rare cases, schizos arent just living day 2 day like theyre k-holing. Tho on the subject of glutamate & dopamines role/relations in schizophrenia, its worth noting that when NMDAR r antagonized, it increases dopamine production/activity as well. its partially y ketamine & ESP memantine r able 2 potentiate p much every drug in existence lol. also, excessive dopamine in neurotoxic, even w/o drugs. so if ur schizo & have chronically high dopamine lvls, u'd be losing neurons & synapses like crazy. which is the most likely reason besides what i mentioned before 2 be dopamine's minor role in hallucinations. but the rsn i mention it is bc schizophrenia is DEFINED almost in modern research science, 2 have significant lacks of synaptic pruning, & excess neurogenesis/neurotrophic factors. ironically much like autism spectrum disorders, which is ac2ly my personal theory on y certain symptoms & phenotypes of autism spectrum disorders overlap so closely w/ some psychotic spectrum disorders, as well. & y either schizoid pd, schizotypal pd, schizoaffective, schizophrenia, & bipolar type 2 + BPD r noteworthily common overlapping disorders w/ ASD. NMDA antagonists notoriously PROTECT neurons & synapses (as seen w/ memenatine in both MDMA & methamphetamines), & this is bc glutamate is the primary neurotransmitter which caninduce SYNAPTIC PRUNING where old synapses between neurons can weaken or die, leading 2 learning & escaping old patterns of behavior, including things like addiction & OCD. but also delusional thoughts. its y d-serine & neboglamine r so fuckin powerful as antipsychotics, even w/o a conjunctive D2 antagonist. it increases d-serine binding & activates NMDAR, further raising extrasynaptic NMDAR, which is quite possibly the most essential subset of NMDAR 4 synaptic pruning, which is unanimous w/ synaptic plasticity & GOOD neurogenesis. u wanna kill old bad connections/synapses in the brain, then regulate/optimize neurotransmitter function & lvls in the brain 2 a healthy homeostasis, then V BRIEFLY, & ESP SELECTIVELY, induce neurogenesis in the hippocampus & amygdala 2 reconsolidate these new, healthy connections between neurons & synapses. what happens 2 a schizo meth addict besides becoming more schizo? which btw, despite meth also raising glutamate bc im sure ur prolly thinking that rn too, its important 2 understand that both NMDAR & dopamine feed in2 each other, so shcizophrenia is kinda like, 2 make an analogy here, 2 dysfunctional ppl getting in an emotionally intense & toxic relationship 2gether where they both simultaneously stay stagnant & dysfunctional due 2 their mutual codependency grown bc of how naturally they work 2gether in the times where things r going good. so the schizo meth addict is low on dopamine all the time, D2 receptors r profoundly downregulated so excessive dysnfunctional firing isnt occuring. but still they have psychosis w/ hallucinations. sure, a small percentage of this is likely influenced by neurotoxicity 2 dopamine neurons as established earlier can happen, but except in v rare cases, NEVER 2 da degree u'll see in the avg dysfunctional schizoprenic patient's episodes of psychosis w/ visual & auditory hallucinations. its glutamate. itssss gluuttaammattteee. bc most D2 abtagonist antipsychotics also profoundly reduce symptoms of mania w/o psychosis or hallucinations like in BPD or bipolar disorder type 1, as well as interestingly autism agression w/ risperiodone specifically (the only FDA approved that has ANYTHING 2 do w/ autism @ all, & also even a bit rarely 4 insomnia. decreasing any extreme excitatory neurotransmitter in excess wil result, again, in a decrease of all brain activity. dopamine is more than just pleasure & motivation, its an essential neurotransmitter 4 consciousness 2 even exist in any meaningful or functional way @ all. this is y parkinons is so debilitating & deadly of a disorder. it, like acetylcholine, which is y both alzheimers/dementia, & deliriant trips fuck u up SOOOOO heavy, & y antipsychotics will literally make u pass tf out. they so necessary 2 process things, both internally & externally. again 4 just an analogy. take a benzo during a nightmare acid trip, wow now suddenly despite being 1 w/ all seconds ago u r barely conscious & can think 2 damn words @ a time & laugh like a retard. but dopamine is also insanely stimulatory, & works in perfect tandem w/ norepinephrine & noradrenaline, so ur bitch ass is gonna be able 2 move, talk, etc. prolly just fine. but glutamate is essential 4 differenting the internal from the external. so a dysfunction here can make u incredibly detached from anything outside of the internal, & the eternal world w/o the ability of discernment or familiarity is a v strange & bizarre place, while being fed all these insane, grandiose, fantastical, or terrifying/bizarre information, & u cant discern from ur detachment/dissociation system essentially lol, has been greatly dampened. this can make every thought seem like ABSOLUTE fact, & theres no reaon 2 question it bc NMDAR hypfunction can also cause a decrease in cholinergic function, which is essential 2 cognition, memory, learning, & logic/complex ideas or tasks. its y nicotine helps w/ schizophrenia btw !!! so ur not learning, not thinking logically, have a dampened memory, the pt of ur brain which is necessary 4 both helping separate fact from fantasy as well as kill "bad" neurons upon coming 2 & realizing ur being crazy rn is hardly functioning the way it needs 2 2 be in tune w/ reality, & ur dopamine is so goddamn high, which ur NMDAR dysfunction is simultaneously enabling the severity of, which is leading u 2 believe as this grandiose & fascinating/interesting topics which can lead u motivated down rabbit holes internally or externally like conspiracy autist schizos or persecutory delusional/grandiose schizos, & its all just not being filtered thru rationality, & the degree @ which ur internal world has become ur entire reality due 2 detahcment, persecution from others 4 said detachment & unpredictability (dopamine in excess causes sudden and erratic behavior), then ur short term memory is fuckt 2 shit & ur logic & rational thinking skills r severely impaired, as well. its the perfect, terrifyingly tragic & macabre storm that acts almost symbiotically 2 help it survive. & these internal worlds r as real & rational 2 the sufferer of these psychotic disorders as this world rn is 2 all of us not tripping or in psychosis rn. its fuckt, & schizophrenia causes the development of sm other debilitating disorders like personality disorders, anxiety, depression. etc. bc of how reinforcing it all is. sorry 4 all of this btw im on meth rn & got hyperfocused on this thought but i think im done now unless yall light the fire under my again by engaging in any way w/ it LOL