Starting to work on an artifical brain for fun.

I could use any help with this one. It’ll be fun. We can zoom and discuss the paramaters of what’s based on the various sciences as well as figure out next steps to completion. This is pulled all over from the net and I was unable to think to get references. Sorry. If some of this is yours, please let me know, unless I know I’ve written it of course. Most of this is wikipedia.

July 18th, 2020: Building an artificial Brain Day 1.

Learn every Cell type in Body and their related functions to figure out how to build the house. 

https://en.wikipedia.org/wiki/Terminologia_Histologica

Medical Subject Headings (MeSH)






Questions:

Ca^++ needs two electrons to be neutral and four electrons taken for Ca^++, so do they both come from the same level of electrons, or is one pulled from the outer shell and an inner shell?

https://www.youtube.com/watch?v=iaRnDULqesc

By removing the 4 electrons you get the noble gas Krypton [Krypton light has many spectral lines, and krypton plasma is useful in bright, high-powered gas lasers (krypton ion and excimer lasers), [Krypton light has many spectral lines, and krypton plasma is useful in bright, high-powered gas lasers (krypton ion and excimer lasers), each of which resonates and amplifies a single] equivalent. But in the brain does it turn into that or just turn into the Noble Ca^++ or NCa^++. Either way it explains why the Nucleus is able to house and withhold the inner workings because it becomes partially back filled with a gaseous substance (or perhaps liquid dense) and is absorbed by the other section firing the Neuron(check to see if at Synapse instead). This process must build a voltage to get the change needed to fire the chemical through.


Main Collective:

Different Lengths of “Fibrous Material”

Binary chemically.
1 Micrometer = 1000 Nanometers = 1,000,000 Picometers.

Bond lengths:
PCO dually 134, PCO Single 154, PCO triple 120:

Oxygen Single, Oxygen 7, 

Doped Si ^3/^-1: 

Perhaps wrap Myelin sheath in doped silicon and then the outer casing can be PCO to allow brain connectivity. 

Doesn’t matter how long the axon is as it can always be made to length per persons need, with varied adjustment from child to adults height. 

Initial Thoughts:

0: PCO encasement to allow safe harbor within the brain. Passed the .9nm BBB issue. 

1:Soma: 25,000,000 picometers.
3:Axon up to a meter, or 1,000,000,000,000 picometers.
2: Terminal Buttons.

Deep Dive:

Soma

Plain PCO would need 91,912 average pieces to create two side of the enveloping sides of the cell wall, plus or minus some amount for the nucleus itself.
Axon would need to have up to 3,676,470,589 pieces to reach a metre so it will hopefully be much less than that.

All synapses have common characteristics, which can be summarized in this list:

  • presynaptic element.
  • neurotransmitter (packaged in vesicles): 
Synaptic vesicle

Neuron A (transmitting) to neuron B (receiving). 1Mitochondria; 2. Synaptic vesicle with neurotransmitters; 3. Autoreceptor 4Synapse with neurotransmitter released (serotonin); 5. Postsynaptic receptors activated by neurotransmitter (induction of a postsynaptic potential); 6Calcium channel; 7Exocytosis of a vesicle; 8. Recaptured neurotransmitter.
Synapse diag1.svg
DetailsA-dynamin-1–dynamin-3–and-clathrin-independent-pathway-of-synaptic-vesicle-recycling-mediated-by-elife01621fs001.jpg Yellow filled up with purple, which activates green from the lower |right side| which looks to implode and pass along materials. 
SystemNervous system
Identifiers
Latinvesicula synaptica
MeSHD013572
THH2.00.06.2.00004
Anatomical terms of microanatomy [edit on Wikidata]

Synaptic vesicles contain two classes of obligatory components: transport proteins involved in neurotransmitter uptake, and trafficking proteins that participate in synaptic vesicle exocytosis (exit from the intercellular walls), endocytosis, and recycling (at which percentage).

  • Transport proteins are composed of proton pumps


    [Look up TP and ADP, Pi, concentrations. Potassium+, Sodium+. I think that once the concentration levels hit a certain level then they flip or switch allowing the chemical change, (look out)]

[Carrier proteins are proteins involved in the movement of ions, small molecules, or macromolecules, such as another protein, across a biological membrane.[1] Carrier proteins are integral membrane proteins; that is, they exist within and span the membrane across which they transport substances. The proteins may assist in the movement of substances by facilitated diffusion (i.e., passive transport) or active transport. These mechanisms of movement are known as carrier-mediated transport.[2] Each carrier protein is designed to recognize only one substance or one group of very similar substances. Research has correlated defects in specific carrier proteins with specific diseases.[3] A membrane transport protein (or simply transporter) is a membrane protein[4] that acts as such a carrier. ]

A vesicular transport protein is a transmembrane or membrane associated protein. It regulates or facilitates the movement by vesicles of the contents of the cell.[5] 

  • that generate electrochemical gradients, which allow for neurotransmitter uptake, and neurotransmitter transporters that regulate the actual uptake of neurotransmitters. The necessary proton gradient is created by V-ATPase, which breaks down ATP for energy. Vesicular transporters move neurotransmitters from the cells’ cytoplasm into the synaptic vesicles. Vesicular glutamate transporters, for example, sequester glutamate into vesicles by this process.
  • Trafficking proteins are more complex. They include intrinsic membrane proteins, peripherally bound proteins, and proteins such as SNAREs. These proteins do not share a characteristic that would make them identifiable as synaptic vesicle proteins, and little is known about how these proteins are specifically deposited into synaptic vesicles. Many but not all of the known synaptic vesicle proteins interact with non-vesicular proteins and are linked to specific functions.[4]

The stoichiometry for the movement of different neurotransmitters into a vesicle is given in the following table.

Neurotransmitter type(s)Inward movementOutward movement
norepinephrine, dopamine, histamine, serotonin and acetylcholineneurotransmitter+2 H+
GABA and glycineneurotransmitter1 H+
glutamateneurotransmitter + Cl1 H+

Recently, it has been discovered that synaptic vesicles also contain small RNA molecules, including transfer RNA fragments, Y RNA fragments and mirRNAs.[5] This discovery is believed to have broad impact on studying chemical synapses.

Effects of neurotoxins[edit]

Some neurotoxins, such as batrachotoxin, are known to destroy synaptic vesicles. The tetanus toxin damages vesicle-associated membrane proteins (VAMP), a type of v-SNARE, while botulinum toxins damage t-SNARES and v-SNARES and thus inhibit synaptic transmission.[6] A spider toxin called alpha-Latrotoxin binds to neurexins, damaging vesicles and causing massive release of neurotransmitters.

Vesicle pools[edit]

Vesicles in the nerve terminal are grouped into three pools: the readily releasable pool, the recycling pool, and the reserve pool.[7] These pools are distinguished by their function and position in the nerve terminal. The readily releasable pool are docked to the cell membrane, making these the first group of vesicles to be released on stimulation. The readily releasable pool is small and is quickly exhausted. The recycling pool is proximate to the cell membrane, and tend to be cycled at moderate stimulation, so that the rate of vesicle release is the same as, or lower than, the rate of vesicle formation. This pool is larger than the readily releasable pool, but it takes longer to become mobilised. The reserve pool contains vesicles that are not released under normal conditions. This reserve pool can be quite large (~50%) in neurons grown on a glass substrate, but is very small or absent at mature synapses in intact brain tissue.[8][9]

Physiology[edit]

The synaptic vesicle cycle[edit]

The events of the synaptic vesicle cycle can be divided into a few key steps:[10]

1. Trafficking to the synapse

Synaptic vesicle components are initially trafficked to the synapse using members of the kinesin motor family. In C. elegans the major motor for synaptic vesicles is UNC-104.[11] There is also evidence that other proteins such as UNC-16/Sunday Driver regulate the use of motors for transport of synaptic vesicles.[12]

2. Transmitter loading

Once at the synapse, synaptic vesicles are loaded with a neurotransmitter. Loading of transmitter is an active process requiring a neurotransmitter transporter and a proton pump ATPase that provides an electrochemical gradient. These transporters are selective for different classes of transmitters. Characterization of unc-17 and unc-47, which encode the vesicular acetylcholine transporter and vesicular GABA transporter have been described to date.[13]

3. Docking

The loaded synaptic vesicles must dock near release sites, however docking is a step of the cycle that we know little about. Many proteins on synaptic vesicles and at release sites have been identified, however none of the identified protein interactions between the vesicle proteins and release site proteins can account for the docking phase of the cycle. Mutants in rab-3 and munc-18 alter vesicle docking or vesicle organization at release sites, but they do not completely disrupt docking.[14] SNARE proteins, do not appear to be involved in the docking step of the cycle.[citation needed]

4. Priming

After the synaptic vesicles initially dock, they must be primed before they can begin fusion. Priming prepares the synaptic vesicle so that they are able to fuse rapidly in response to a calcium influx. This priming step is thought to involve the formation of partially assembled SNARE complexes. The proteins Munc13, RIM, and RIM-BP participate in this event.[15] Munc13 is thought to stimulate the change of the t-SNARE syntaxin from a closed conformation to an open conformation, which stimulates the assembly of v-SNARE /t-SNARE complexes.[16] RIM also appears to regulate priming, but is not essential for the step.

5. Fusion

Primed vesicles fuse very quickly in response to calcium elevations in the cytoplasm. This fusion event is thought to be mediated directly by the SNAREs and driven by the energy provided from SNARE assembly. The calcium-sensing trigger for this event is the calcium-binding synaptic vesicle protein synaptotagmin. The ability of SNAREs to mediate fusion in a calcium-dependent manner recently has been reconstituted in vitro. Consistent with SNAREs being essential for the fusion process, v-SNARE and t-SNARE mutants of C. elegans are lethal. Similarly, mutants in Drosophila and knockouts in mice indicate that these SNARES play a critical role in synaptic exocytosis.[10]

6. Endocytosis

This accounts for the re-uptake of synaptic vesicles in the full contact fusion model. However, other studies have been compiling evidence suggesting that this type of fusion and endocytosis is not always the case.

Vesicle recycling[edit]

Two leading mechanisms of action are thought to be responsible for synaptic vesicle recycling: full collapse fusion and the “kiss-and-run” method. Both mechanisms begin with the formation of the synaptic pore that releases transmitter to the extracellular space. After release of the neurotransmitter, the pore can either dilate fully so that the vesicle collapses completely into the synaptic membrane, or it can close rapidly and pinch off the membrane to generate kiss-and-run fusion.[17]

Full collapse fusion[edit]

It has been shown that periods of intense stimulation at neural synapses deplete vesicle count as well as increase cellular capacitance and surface area.[18] This indicates that after synaptic vesicles release their neurotransmitter payload, they merge with and become part of, the cellular membrane. After tagging synaptic vesicles with HRP (horseradish peroxidase), Heuser and Reese found that portions of the cellular membrane at the frog neuromuscular junction were taken up by the cell and converted back into synaptic vesicles.[19] Studies suggest that the entire cycle of exocytosis, retrieval, and reformation of the synaptic vesicles requires less than 1 minute.[20]

In full collapse fusion, the synaptic vesicle merges and becomes incorporated into the cell membrane. The formation of the new membrane is a protein mediated process and can only occur under certain conditions. After an action potential, Ca2+ floods to the presynaptic membrane. Ca2+ binds to specific proteins in the cytoplasm, one of which is synaptotagmin, which in turn trigger the complete fusion of the synaptic vesicle with the cellular membrane. This complete fusion of the pore is assisted by SNARE proteins. This large family of proteins mediate docking of synaptic vesicles in an ATP-dependent manner. With the help of synaptobrevin on the synaptic vesicle, the t-SNARE complex on the membrane, made up of syntaxin and SNAP-25, can dock, prime, and fuse the synaptic vesicle into the membrane.[21]

The mechanism behind full collapse fusion has been shown to be the target of the botulinum and tetanus toxins. The botulinum toxin has protease activity which degrades the SNAP-25 protein. The SNAP-25 protein is required for vesicle fusion that releases neurotransmitters, in particular acetylcholine.[22] Botulinum toxin essentially cleaves these SNARE proteins, and in doing so, prevents synaptic vesicles from fusing with the cellular synaptic membrane and releasing their neurotransmitters. Tetanus toxin follows a similar pathway, but instead attacks the protein synaptobrevin on the synaptic vesicle. In turn, these neurotoxins prevent synaptic vesicles from completing full collapse fusion. Without this mechanism in effect, muscle spasms, paralysis, and death can occur.

“Kiss-and-run”[edit]

The second mechanism by which synaptic vesicles are recycled is known as kiss-and-run fusion. In this case, the synaptic vesicle “kisses” the cellular membrane, opening a small pore for its neurotransmitter payload to be released through, then closes the pore and is recycled back into the cell.[17] The kiss-and-run mechanism has been a hotly debated topic. Its effects have been observed and recorded; however the reason behind its use as opposed to full collapse fusion is still being explored. It has been speculated that kiss-and-run is often employed to conserve scarce vesicular resources as well as being utilized to respond to high-frequency inputs.[23] Experiments have shown that kiss-and-run events do occur. First observed by Katz and del Castillo, it was later observed that the kiss-and-run mechanism was different from full collapse fusion in that cellular capacitance did not increase in kiss-and-run events.[23] This reinforces the idea of a kiss-and-run fashion, the synaptic vesicle releases its payload and then separates from the membrane.

Modulation[edit]

Cells thus appear to have at least two mechanisms to follow for membrane recycling. Under certain conditions, cells can switch from one mechanism to the other. Slow, conventional, full collapse fusion predominates the synaptic membrane when Ca2+ levels are low, and the fast kiss-and-run mechanism is followed when Ca2+ levels are high.

Ales et al. showed that raised concentrations of extracellular calcium ions shift the preferred mode of recycling and synaptic vesicle release to the kiss-and-run mechanism in a calcium-concentration-dependent manner. It has been proposed that during secretion of neurotransmitters at synapses, the mode of exocytosis is modulated by calcium to attain optimal conditions for coupled exocytosis and endocytosis according to synaptic activity.[24]

Experimental evidence suggests that kiss-and-run is the dominate mode of synaptic release at the beginning of stimulus trains. In this context, kiss-and-run reflects a high vesicle release probability. The incidence of kiss-and-run is also increased by rapid firing and stimulation of the neuron, suggesting that the kinetics of this type of release is faster than other forms of vesicle release.[25]

Solutions (Possible):

  • synaptic cleft.

Insulator phase:
PCO Outer core to allow safe reinforcement of synapses as well as inner core being an insulator that allows for difference between what happens with the inside the synapses and what happens within the cell walls to allow them to attach. You may only need one type as PCO is sticky in nature (I believe)

  • receptor proteins.
  • postsynaptic element.
  • neurotransmitter breakdown or re-uptake.

2200km/sec = 7217848 ft/sec.
Regardless of current average heights it takes less than a second to perform the action taken of a synapse. 

Adult:

(8 ft) / (7 217 848 (ft / second)) =

1,108.3636 nanoseconds

Birth Child Fully Formed:

(19 inches) / (7 217 848 (ft / second)) =

219.363629 nanoseconds



Bond Lengths:
PCO: 140+134 = 274 ish PicoMeters Radii.
Doped Si = 111 pm radii.

Ca^++ = 231 pm radii. First Chemical to look out for.
 

Neurotransmitters:
Chloride^- or Potassium^+ from gamma-Aminobutyric acid [GABA]

Dendrite Mapping to Upstream/side stream neurons. 


Cellular Batteries:
Molecular pumps that pull potassium into cells and push sodium out create a chemical battery

Internal Battery Usage from within the cell:
In the cerebral cortex of mice, about a quarter of the brain’s energy goes to maintaining the neurons and glial cells themselves — the processes that all cells go through to remain alive. The remaining 75 percent is used for signaling. So with the added space we could increase the battery life and make memories last longer, hopefully without repercussions as minor time dilation as the world slows down around you. For all I know consciousness is electricity based at the moment and futzing with the speed (known the given limitation of an electron down the right pathways minimized) changes the users perception. 

Formatting the project:


You could: Go chemical to chemical and build it out for everyone.
You could: Describe it to everyone in minute detail.
You could: Describe it to everyone in lesser detail. Until asked, then provide imagery as you have done so before.

Let’s go long format and condense at end:

Parts of the Synapse:

Neurotransmitters:

What are the 7 neurotransmitters?

Understanding 7 Major Neurotransmitters

  • Glutamate. This amino acid is common in your diet. …
  • GABA (γ-aminobutyric acid) If glutamate is the most excitatory chemical messenger, then GABA is its polar opposite. …
  • Dopamine. …
  • Adrenaline (Epinephrine) …
  • Serotonin. …
  • Oxytocin. …
  • Acetylcholine.

The cerebrum

The cerebrum, the large, outer part of the brain, controls reading, thinking, learning, speech, emotions and planned muscle movements like walking. It also controls vision, hearing and other senses.

The cerebrum is divided two cerebral hemispheres (halves): left and right. The right half controls the left side of the body. The left half controls the right side of the body.

Each hemisphere has four sections, called lobes: frontal, parietal, temporal and occipital. Each lobe controls specific functions. For example, the frontal lobe controls personality, decision-making and reasoning, while the temporal lobe controls, memory, speech, and sense of smell.

Parietal Lobe controls:

Occipital Lobe controls:

The cerebellum

The cerebellum, in the back of the brain, controls balance, coordination and fine muscle control (e.g., walking). It also functions to maintain posture and equilibrium.

The brain stem

The brain stem, at the bottom of the brain, connects the cerebrum with the spinal cord. It includes the midbrain, the pons, and the medulla. It controls fundamental body functions such as breathing, eye movements, blood pressure, heartbeat, and swallowing.

but more than 200 have been identified.
Average Range of Sizes known is that a good estimate of the size of neurotransmitters would be from around 0.5 to 5 nanometers or 500 – 5,000 picometers.

Basic Chemistry:

Lets start slowly with the seven major Neurotransmitters sizes:

Amino Acid is roughly 10nm or 10,000 picometers.

ReceptorsNMDA, AMPA, kainate, mGluR
AgonistsNMDA, AMPA, kainic acid
AntagonistsAP5, ketamine, CNQX, kynurenic acid
Precursormainly dietary sources
Metabolismglutamate dehydrogenase


GABA (γ-aminobutyric acid) If glutamate is the most excitatory chemical messenger, then GABA is its polar opposite. …

In vertebrates, GABA acts at inhibitory synapses in the brain by binding to specific transmembrane receptors in the plasma membrane of both pre- and postsynaptic neuronal processes. This binding causes the opening of ion channels to allow the flow of either negatively charged chloride ions into the cell or positively charged potassium ions out of the cell. This action results in a negative change in the transmembrane potential, usually causing hyperpolarization.

Dopamine:


Adrenaline (Epinephrine):

If added in small doses so that they increase memory you could essentially build synapses that give photographic memory similar to your own (as it used to be before the psychosis) 


Serotonin: 5-hydroxytryptamine (5-HT) is a monoamine neurotransmitter

Oxytocin:

https://en.wikipedia.org/wiki/Oxytocin
Check out the links provided with the Chemicals. 

Acetylcholine:

Do it just for the sake of doing it.


Okay after some thought it seems like doing a chain of events is the best way to get it sorted. It’s probably been done but I’ll take a quick look and see so, and if not, will spend tonight doing that.

Neurotransmitter  Controls what with which chemical(s)
AcetylcholineMuscles. With 



Start a conversation if they’ll have it.