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So, I recently got interested in neuroscience and decided to learn more. Having had no formal training in neurobiology before, I just registered for this course on Coursera.
coursera.org/learn/neurobiolog
Let's see how it goes.

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There's only one type of neurons that leaves the central nervous system (CNS) and goes directly to muscles, and that's the motor neuron.
There are a hundred thousand out of 200B neurons in the CNS.
The motor neurons are contained either in the brain stem or in the spinal chord. But, there are no motor neurons in the forebrain.

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Perception -- the conscious perception of sensory inputs, the conscious appreciation of sensory inputs -- depends entirely on the forebrain.
The conscious appreciation of sensory inputs depends on the cerebral cortex.

Homeostasis is a distributed process, which depends on forebrain, brain stem and spinal chord.
The contribution of forebrain to homeostasis is hormonal. The contribution of brain stem is through autonomic changes (changes we are not consciously in control of) as well as through consciously made movements.
Same is true for spinal chord.

Higher Abstract Functions depend entirely on forebrain.

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Neurons have four parts. The first is the cell body, also called the Soma. And this is the part that all cells have, this is cell central.

The cell body has coming out it from a number of dendrites, and these dendrites branch. And they continue to branch. And so, that makes a tree which we call the dendritic arbor or the dendritic tree.

And these dendrites are responsible for gathering in information. They're the sentries. They are the ears of the cell, of the neuron. They're taking in all information. So information is going in to the dendrites.

Axon carries the information along the length of it.

Neurons talk to neurons. But neurons also, go talk to muscles. And neurons talk to glands. And neurons talk to the cardiac, to the heart, to the cardiac muscle and so on.

Source of image: courses.lumenlearning.com/boun

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This is the axon and you can see that it gives off these little terminals, and it also has places where there's just simply a swelling on root. So these are all synaptic, these swellings are synaptic terminals. The long slender projection of the nerve cell is an axon.

Image source: screenshot at 5:44 from coursera.org/learn/neurobiolog

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And the anatomy of the neurons is different in appearance. But, it's also different in the sense of what is a neuron connected to, what neurons are talking to it, and what neurons is it talking to. So the inputs and the outputs of each neuron are going to be different.

In addition to the anatomy, the other differences include excitability -- and this is essentially how talkative is the neuron; how much do you have to goad it to get it to say something.
Some neurons are talking all the time; and some neurons are very laconic, very unlikely to speak.

And finally, there's how do they speak? And what we're talking about is the neurotransmitter. What is the neurotransmitter -- or what's the chemical, the substance -- that the neuron uses?

There is also a difference in both speed -- whether is something fast or slow -- or also whether it's affirmative or or negative -- 'yes' or 'no', and how fast does it take you to get to 'yes' or 'no'.

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**Glial Cells**
The human brain contains 86B neurons and 85B Glia.

**Different types of Glia:**

๐Ÿ”ธ Astrocytes: Astrocytes are really important type of Glia. They're essentially responsible for keeping the environment clean, they're the sanitation worker of the brain. So they are picking up all the refuse that the neurons have let loose including excess ions, excess and their metabolites.

They also are very important during development. They allow neurons to get to where they have to go during development. are born in one place and they have to go some place else, and what highway did they take? They hitch on a progenitor cell that is going to become an .

And, in addition when synapses are formed, the synapses are not maintained without some effort, and part of that is that the synapses are enveloped in the processes of . So, there's a lot of structural and metabolic support that the Astrocytes are providing for neurons.

๐Ÿ”ธ Oligodendrocytes and Schwann Cells: The make myelin in the CNS and the make it in the Peripheral Nervous System. So all these demyelinating diseases will affect either central myelin or peripheral . They will not affect both -- central or peripheral.

Because they are made by two different types. The Oligodendrocytes in the central nervous system and a Schwann cells in the peripheral nervous system.

๐Ÿ”ธ Microglia: are the one exception to the rule that
nervous system, that the cells of the nervous system come from Ectoderm. These are actually essentially immune cells coming from the blood lineage. These are immune cells that have invaded into the central nervous system and their job is to be quiet. And if we're healthy and everything goes well, they are quiet. But when there is a problem these microglia react, they try to rectify things, they try and bring some attention to areas of damage and what is emerging is that sometimes they go overboard and they start to participate in making the problem as well as solving the problem.

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๐Ÿง  Myelin is a fatty wrap that goes around some axons.

๐Ÿ”ธ An unmylinated or naked axon can only transfer information at a slow rate. So the rate that it's transfers information is 0.2 to 1 meters per second.

๐Ÿ”ธ Now, once we put on , information transfers much much faster. It can go between 2 and 120 meters per second. If it goes at 120 meters per second, the whole game is over. So very short time, imperceptible to us.

๐Ÿ”ธ That information occurs in a 0 or a 1. There's either a point of information or not. **And so it's very much like a computer code**, where what we're seeing is a series of and what's important, the 0s are less important but the temporal pattern of these ones is very important.

๐Ÿ”ธ And these 'ones' are actually an action potential, also called a spike. And we talk about firing spikes, neurons fire spikes. So, the timing of these spikes is what carries information.

๐Ÿ”ธ The information spikes actually jump. That's what makes it so fast. They don't have to actually be carried through the places; with the , they can actually jump.

๐Ÿ”ธ And now, if we have a , what we're going to end up with is some information that's spread out, because it's slower. And every once in a while, it's going to miss bits.

๐Ÿ”ธ The neuron, that we're talking, to is getting a very incoherent message. This is very different from the original message and that is the problem with demyelination. Because axons are demyelinated, the information transfer is very degraded. It's a garbled message and that's a problem.

Image source: Screen-grab from coursera.org/learn/neurobiolog.

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๐Ÿ”ด Demyelinating Diseases

๐Ÿ”ธ The that make the myelin are of different types that make it (myelin) in the central nervous system and in the peripheral nervous system. And because of that, people who get a demyelinating disease, get it either in the central nervous system or in the peripheral nervous system -- but not in both.

๐Ÿ”ธ So the problem is either in the (and the interaction between the oligodendrocytes and the axon) -- in which case you get a central demyelinating disease, and the most common by far is multiple -- or there's a problem in the and its connection to the axon, and in that case you can get a variety.

๐Ÿ”ธ There are a diverse group of hereditary neuropathies called Charcot-Marie Tooth, which are . They're inherited and they typically progress and become worse with time.
๐Ÿ”ธ There's also an acute demyelinating disease called Guillainโ€“Barrรฉ, which typically has a very quick onset, it's inflammatory, and luckily it goes away after a while.

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๐Ÿ”ธ There's a barrier, a fence that is the demarcation between central and peripheral nervous-systems. And that fence is made up of three membranes, and those three membranes are the 'meninges'.
๐Ÿ”ธ There are three meningeal layers, and the three layers go from very weak, very tender, the pia, to very tough, the dura and, in between, there's a spidery thing called the arachnoid.

๐Ÿ”ธ The only neurons that leave the central nervous system are the neurons that serve a motor function.
They actually go out the meninges and they go into the periphery. In the periphery, there's the peripheral nervous system, and there's also the rest of the body.

๐Ÿ–ผ๏ธ Image Source: thoughtco.com/brain-anatomy-me

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๐Ÿ”ธ The form a very effective barrier against toxins, viruses, against all sorts of damage, so that the peripheral nervous system tends to be far more vulnerable than the central nervous system.

๐Ÿ”ธ In addition, the two regions have very different capacities for repair.

๐Ÿ”ธ If you cut an axon in the peripheral nervous system, it can repair itself -- It will reconnect. If there's a traumatic injury to the central nervous system, the same does not happen. So, the ability to repair is far, far greater in the periphery than in the central nervous system.

๐Ÿ”ธ A large molecule called botulinum toxin, which comes from spoiled food, can get in and it primarily will affect the peripheral; it will only affect the peripheral neurons. It will not get past the meninges.

๐Ÿ”ธ actually gets in right at the synapse between the motor neuron and the voluntary muscle, and it goes back. It travels back and it does a clever thing -- It gets through the meninges, but it gets through the meninges by getting in through an axon of a motor neuron. And what does it do then? For thanks, it actually kills this motor neuron. So now, that motor neuron is going to die.

๐Ÿ”ธ Let's look at another virus: herpes zoster.
Herpes zoster is a virus that produces, what's commonly called as, . And in herpes zoster, the virus gets into the dendrites of sensory neurons, and it gets transported back inside the axon in these sensory neurons, and then it goes and lives in synaptic terminals. And if all is great, it lives in there and then it never talks again.

๐Ÿ”ธ But, under some circumstances, the virus can decide to reproduce and blossom, and it will make copies of itself so that it actually sends it back out. And what you get is a virus all throughout the sensory territory and what you get is a rash.

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๐Ÿง 

๐Ÿ”ธ One source of brain tumors is metastasis -- which are spreads from other tumors, so for instance, lung tumors.

๐Ÿ”ธ The brain tumors are a problem because they exist within the cranium, and the cranium is a fixed, bony container. It can't expand. And as a tumor expands, the cranium is not going to expand. It's going to increase the pressure and we're going to have a problem.

๐Ÿ”ธ Neurons don't make tumors because they don't divide at all, and they don't get into this uncontrolled division. So what makes tumors? Well, it's other cell types within the brain. And the primary one that does this are .

๐Ÿ”ธ Glial cells don't have the limits on division that neurons do. So, glial cells can divide and make these tumors. And so, , tumors of glial cells, are the most common type of brain tumor.

๐Ÿ”ธ Another type of brain tumor is the type that comes from a division of meningeal cells, and these are called .

๐Ÿ”ธ And finally, the other major type of brain tumor is are tumors that come from glandular cells.

๐Ÿ”ธ These glandular cells are not neurons. They're gland cells, and they can divide without control. The other gland that we have in our head is called the pituitary, and these pituitary cells can also divide and that's called 'pituitary adenomas'. These 's are fairly common. They account for about 10 to 25% of inter-cranial tumors.

๐Ÿ–ผ๏ธ Image source: images.app.goo.gl/hfXZKhrd7aha

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: A pineal tumor is a tumor that forms in the pineal gland . The gland is a tiny gland in the middle of your head. It's surrounded by your brain. It makes a hormone called melatonin that affects your sleep-wake cycles. Pineal tumors are very rare tumors. They happen most often to children and to adults younger than 40.
cedars-sinai.org/health-librar

: The exact cause of hypothalamic tumors is not known. It is likely that they result from a combination of genetic and environmental factors.
In children, most hypothalamic tumors are gliomas. Gliomas are a common type of brain tumor that results from the abnormal growth of glial cells, which support nerve cells. Gliomas can occur at any age. They are often more aggressive in adults than in children.
pennstatehershey.adam.com/cont

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The spinal cord and the brain make up the central nervous system.
Foramen magnum is the hole where the spinal cord comes up, and it joins and continues with the brain.
Image source: images.app.goo.gl/77CdugW1ym8M

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๐Ÿง 

๐Ÿง  The dura mater, tough mother, is the most outer layer of the meninges, and inside of that layer is the . And the arachnoid is the filmy-like substance and it covers the entire surface of the brain. It doesn't invaginate with every hill and valley of the brain.
Pia, the final layer of the meninges, is too fine to be seen.

๐Ÿง  The dura is separated from the brain by a layer of fluid, and what that does is that it circles the brain and it in-cases the brain in this bag of fluid. So that, as the brain moves around, it's cushioned -- it can't bang against the skull because it's cushioned by the fluid.

๐Ÿง  In the , the dura is right up against the skull; there's no separation. They can't be separated, except if there's a bleed. And that is a very dangerous situation, that's a medical emergency.
If there's a bleed between the skull and dura. If there's some injury and blood gets in there that's a medical emergency.

๐Ÿง  In contrast to the situation in the cranium, where the dura is right up against the bone, the dura in the spinal cord is not up against the . So there's a lot of space. It's not up against the bone. And therefore, you can imagine that increasing pressure in the cranium is a much bigger deal.

๐Ÿง  If the dura is tough, the dural folds are doubly tough, because they are actually double, double folds -- folds made of two layers of dura.

๐Ÿง  There's a fold called the Falx Cerebri, and it goes between the two parts of the brain, between the two hemispheres.
Tentorium is the dural fold that goes between the cerebrum and the cerebellum.

๐Ÿง  The most important point of these folds, or one of the benefits of these folds, is that they separate problems, pressure problems, into three compartments.

๐Ÿ–ผ๏ธ Image source: in.pinterest.com/pin/191614159

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โšก Electrical language of cells โšก

โš›๏ธ In a living organism, we don't use electrons. Instead, we use molecules that have a charge, and those molecules are called ions.

โš›๏ธ So these ions are present within the context of cells. And all cells have what are called cellular membranes, which are made up mostly of fat. It's important to understand that most of a membrane is fat. And this is like a layer of oil surrounded by a couple layers of water.

โš›๏ธ Let's consider an ion that's positively charged, and let's consider one to be potassium ion (K+).

โš›๏ธ This potassium ion is very happy in water, but it can't get through oil. It's not gonna pass through there. So it's gonna bounce off this membrane. And the only way for it to get through is via a special place which we're gonna call an ion channel.

โš›๏ธ The physical force for this potassium ion is to leave the cell because of lower concentration of ions outside the cell than in the cell (osmosis).
But, on the other hand, the cell is actually negatively charged. And outside the cell is grounded.

โš›๏ธ The potassium ion is positive and so there's an electrical force that attracts it into the cell.

โš›๏ธ The potential at which the physical (osmotic) force and the electrical force will be equal is where the membrane is gonna sit.

โš›๏ธ And we have to worry about three ions -- the potassium ion, the sodium ion, which is also positively charged, and chloride ion. And once we take into consideration each of these ions, what we see is that this cell is going to sit at rest at about -70 to -60 millivolts (with respect to the potential outside the cell).

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โšก Neurons sit at a resting membrane potential of about -65 mV.

โšก Small little potential differences โ€” which are on the order of less than one millivolt up to, say, five millivolts โ€” can travel along the neuron.

โšก They might travel, but they're going to peter out pretty quickly. So, it's not going to work to simply rely on these small potential changes if we have to go long distances.

โšก The longest neuron that we possess is a cell that has a cell body right at the base of the spine. And it sends one process all the way down to the toe, and it sends another process all the way up to the medulla.

โšก Because neurons are so long, we use something called the Action Potential. And the Action Potential goes really far up and comes back down in height. So, it's about 100 mV.

โšก So from the resting memory potential (-65mV) to the top of the Action Potential โ€” which happens at around, say, 20mVs or so โ€” we're talking about roughly 100 millivolts of difference. And that can get communicated all the way up. That's not going to get lost.

โšก And what carries that Action Potential is: โ€”
We looked at potassium being in very high concentration in a cell and much lower outside a cell. The reverse is true for sodium.
And so, the sodium comes flooding in, and because it's positively charged, that's what takes the cell up to this very high membrane potential.

โšก Now the ability for a neuron to communicate using an Action Potential is a slow process unless we add one more thing, and that is an insulator โ€”essentially a very nice insulator โ€”called myelin.

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๐Ÿงซ The synaptic terminal has these entities here, which are called synaptic vesicles, and they're small, little organelles.

๐Ÿงซ They're little vesicles made of a membrane; just like the cell has a cell membrane, these vesicles have a vesicular membrane.
The neurotransmitters are within the vesicular membrane.

๐Ÿงซ And, the neurotransmitter can be any number of a number of different molecules โ€” , , , , , , , , , .

๐Ÿงซ The neurotransmitters are packaged in vesicles. The second thing that's important about this is that we can use the synthesis of a as a therapeutic tool.

๐Ÿงซ So, for instance, Dopamine is missing in .
It's not that dopamine isn't made per say, that's there's a problem with making it โ€” it's that the cells that make it die.

๐Ÿงซ There's something called 'Mass Effect', which means that you take the starting chemical (the substrate) and then through a series of enzymatic processes reaction, through a series of enzymatic reactions, we end up with a neurotransmitter.

๐Ÿงซ In the case of Dopamine, what we do to treat in most people with Parkinson's is that we give them the substrate โ€” and so that (drug) is what is commonly known as or .

๐Ÿงซ So we flood the system with substrate, and the goal is to get a little bit of that neurotransmitter out of the system.

Image source: in.pinterest.com/pin/119627552

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๐Ÿ”ธ How do we get the neurotransmitter out of the vesicle and out of the cell and make it able to go and affect another cell?

๐Ÿ”ธ There is a cell membrane, but the cell also has a lot of other membranes that are inside. Inside in these things called organelles.

๐Ÿ”ธ The fusion between two different membranes happens constitutively. And the challenge for a neuron is to stop that.
We can't have these vesicles fusing with the plasma membrane, with the cell membrane all the time. That would not work.

๐Ÿ”ธ What we want to do is we want to make the vesicle fuse to the membrane **only when the action potential arrives** .

๐Ÿ”ธ So the key to neurotransmitter release is two things:
1. We're going to suppress constitutive or ongoing release.
2. We are going to link the release that we want in the synaptic terminal to the action potential.

๐Ÿ”ธ There is a molecule that suppresses constitutive release within the synaptic terminal.

๐Ÿ”ธ When the action potential comes in, the membrane potential increases and it opens a particular type of ion channel that lets in calcium ions.

๐Ÿ”ธ These are positively charged ions with two positive charges. And, these calcium ions are going to flood in to the synaptic terminal, and that is going to trigger release.

๐Ÿ”ธ The release that happens of vesicles that contain neurotransmitters is only when the calcium concentration increases.

๐Ÿ”ธ All that happens when the calcium concentration increases is that the vesicular membrane and the the cell membrane fuse.
And the calcium concentration only increases when the action potential arrives.

๐Ÿ–ผ๏ธ Image source: screen-grab from coursera.org/learn/neurobiolog

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Clostridial Toxins:

๐Ÿ”ธ Botox is one of several clostridial toxins made by clostridial bacteria. And the full name of Botox is actually botulinum toxin.

๐Ÿ”ธ The vesicles are held very close to the cell membrane. What holds them? A group of three proteins, two of them anchored in the cell membrane, one of them anchored in the vesicle membrane. This complex is called the snare complex.

๐Ÿ”ธ And what happens when calcium comes in is that it changes snare complex's shape. Caยฒโบ changes snare's configuration to being in a straight line. [see GIF]

๐Ÿ”ธ So that pushes the vesicle into the plasma membrane and fusion Is inevitable. It takes a lot of energy for them not to fuse, and when they're that close, it's inevitable.

๐Ÿ”ธ It's the snare pin's sensitivity to calcium that is the final event that allows the vesicle to fuse with the cell membrane.

๐Ÿ”ธ Botox comes in and cuts a particular protein of these proteins of the snare pin. But the clostridial toxins cut a variety of places in these three proteins that make up the snare pin.

๐Ÿ”ธ If the snare pin is broken for whatever reason, if that is cut, then release doesn't happen.

๐Ÿ”ธ Nowadays, we use clostridial toxins all the time โ€” and we use them for very serious problems, such as focal dystonia, where there is an inappropriate continual contraction of a muscle, and that is a basal ganglia disorder.

๐Ÿ’‰ So, the Botox is injected at a very low dose, very locally.
And Botox is used for a large variety of treatments of various disorders. It's also used cosmetically.

๐Ÿ”ธ And the interesting thing about it's use in cosmetics is that, before the widespread use of Botox, we made our own wrinkles. And what Botox is doing is preventing the motor neuron from releasing the neurotransmitter on to the muscle, and thereby preventing us from actively making our own wrinkles.

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๐Ÿ”ธ Motor neurons are a very special type of neuron. If they die, you can no longer move muscles.

๐Ÿ”ธ The motor neurons are contained either in the brain stem or in the spinal cord. But, there are no motor neurons in the forebrain.

๐Ÿ”ธ So the motor neurons in the brain stem move the face, move the mouth, move the larynx, and are responsible for speech and swallowing, facial expressions, things like that.

๐Ÿ”ธ The motor neurons in the spinal cord are responsible for movements of all the arms, our legs, our trunk. All of our movement that we do with our body happens through the spinal cord.

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