I'M MAKING A DRUG THAT INCREASES IQ (95 -> 193)

[Grin2b No.14678604]

D21 was discovered by researchers studying the relationships of dopamine1 and dopamine2 receptors forming a heterodimer. D1 and 2 receptors have seemingly opposing activity with D1 being excitatory and D2 being inhibitory
The dopamine1-2 heterodimer is a pseudo-receptor whose expression increases as a consequence of dopamine1 and dopamine2 receptors being targeted and activated at the same time
This receptor binds a large portion of D1 and 2 receptors together and prevents them from functioning properly so both excitatory and inhibitory dopamine activity is reduced
When this heterodimer is activated, rewards from activities are greatly reduced and the satisfaction from that reward is reduced (a hedonic appetite)
This is bad in the context of long-term potentiation and in long-term depression where we attempt to learn new concepts because in the concept of dopamine signaling D1 is the reward and D2 is the anti-reward. So If you're anticipating a certain response when learning and you get a wrong answer then D2 exerts this long-term depression or reduced activity in response to an unsatisfactory result and so you don't learn something that is not beneficial.
The heterodimer increases with age, or with mental disorders or drug use and this acts as a brake on further learning, reduces plasticity, and is a contributor to the end of the critical period from adolescence.
It may be an evolutionary adaptation that promotes specialization in individuals and locking in learned memories and survival skills from childhood because it may have been bad for aged humans to compete for resources with younger humans for resources.
The researchers that discovered d21 went through a lot of effort to determine the epigenetic signature of the heterodimer and they copied the DNA sequence of this receptor and then they cut out or replaced that segment so they had a full protein that then prevented this dimer from freeing dopamine receptors so that you have a younger dopamine phenotype

[Anonymous No.14678610]

k

[MASTER SKIPPER No.14678740]

>>14678604
IQ is contingent on brain tissue anatomy, you brainlet. Altering neurotransmitters wil confer marginal improvement.

[Grin2b No.14680430]

>>14678740
Dopamine is heavily implicated in learning, see Berke, J.D. What does dopamine mean?. Nat Neurosci 21, 787–793 (2018).
D21 peptide, by virtue of removing the d1d2-heteromer, obviously would heavily promote plasticity. Talk about being clueless, maybe you should skip less classes.

[Anonymous No.14680449]

>>14678740
Not him, and not arguing his point, but altering neurotransmitters can make you significantly more motivated to pursue a task and develop neural pathways that make you more intelligent in pursuing that and similar tasks.

[Anonymous No.14680464]

>>14678740
Dumbfuck. This isn't merely "altering neurotransmitters", this is restoring younger states of neurotransmitters that are obviously more effective.

[Anonymous No.14680471]

Dopamine1 is what is more closely tied to LTP and shares a strong relationship to nmda signalling which is generally thought of as a coincidence detector.
Dopamine1 activity is greatly raised in response to reward and that induces LTP and the formation of stronger connections to other neurons which would then fire alongside it.
The dopamine heterodimer increases with age, or with mental disorders or drug use for example and this acts as a brake on further learning and functionally reduces plasticity and its a contributor to the end of the critical period from adolescence.
So the dimer makes dopamine 1 and 2 receptors behave in a odd fashion because its activity suppresses new learning and contributes to anxiety and depression because it sort of acts to maintain the status quo and that prevents dopamine from acting properly.

[Pax !!xgt+XatlhjD No.14680473]

Our body has a large proportion of hylauronic acid receptors especially within the nose and this allows the peptide to bind to the hylauronic acid receptor and be carried much deeper into the brain than the peptide itself may be transported intranasally alone. Hylauronic acid also greatly reduces the enzymatic degradation of this peptide and likely reduces the dose needed by a large amount. Cogmetics IIRC also had made a requirement to the peptide lab to make the D21 peptide with all D amino acids. He had been working with L amino acids at one point i believe and asked the lab to throw it out. D amino acids would make this peptide have much greater enzymatic degradation resistance and so when the conjugation is finished we would in reality have a drug that is far derived from D21 that researchers have worked with in the past and would free up heterodimers in the entire brain and even in the periphery as well.
because we have nerve cells throughout the periphery in our organs, muscle, blood vessels and under the skin this would free up more dopamine sensitive cells through our entire body and likely have large overarching effects through increasing insulin sensitivity, controlling blood pressure, osmotic balance in our kidneys its likely that d21 would do amazing things that go well beyond just the brain and would likely control inflammation as well especially if you're looking at neuroendocrine functions of the hypothalamus

[Pax !!4OAhmib8eZP No.14680477]

deferoxamine is giving me the effects that i'd anticipate to come from d21. Since it seems apparent that the d1-d2 heterodimer is highly present in adhd, ASD, Schizophrenia, drug addiction and increases during the progression of aging it seems that the heterodimer forms as a consequence of iron dysbiosis, either both iron deficiencies from within mitochondria and iron overload in the cytosol interferes with mitochondrial atp production and anterograde mitochondrial transport to synaptic vesicles and this significantly reduces synaptic density. It would also explain the internalization of synaptic nmda subunits and increased expression of extrasynaptic nr2b. Reduced oxidative respiration of mitochondria would lead to the failure of atp production and excitotoxicity as a consequence of mitochondrial pore potential. This could be the link between cognitive dysfunction present in disorders of iron deficiencies and iron overload.
Would you anticipate a failure in iron proteostasis would lead to the formation of the D1-D2 heterodimer?

[Anonymous No.14680490]

>>14678604
How do you prevent the supersmart psychopaths from killing you (and getting away with it?

A smart self-serving individual will have better chances at procreating than an equally smart altruistic person.