You Won’t Believe When You Get To Know About What Do Neurons Actually Do?
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You Won’t Believe When You Get To Know About What Do Neurons Actually Do?

It is general knowledge that our brain is a combination of neurons. What are neurons? Well, those are building blocks of the brain. We may also recognize neurotransmitters, magic chemicals, neurons use to communicate. Neurons create complex emotions and memories using these chemicals. How do they do this?

For starters, a neuron is the functional unit of the brain. Because it plays a role in sensory, reflexive, and motor functions and memory formation.

Neurons are diverse. They come in all sizes. In fact, over 1,000,000 types of neurons exist and so they’ve never faced division of categories. We just divide them into three vast groups. Later, you’ll find out about these groups. For now, remember this: All these neurons share a common basic structure.

A neuron comprises three parts: cell body, axon, and dendrites. The cell body is like any other cell. The cell body contains the nucleus which controls all cell function; mitochondria, which play a role in energy production for metabolic activities; ribosomes, where protein synthesis occurs; and other usual cell organelles. The axon is a filament-like extrusion that extrudes from the cell. Its unique appearance distinguishes it from dendrites. A neuron can have only one axon. Dendrites are other such extrusions, distinct from the axon. A neuron can have many dendrites. But remember: Every neuron has only one axon.

What is a neurotransmitter? 

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Image Source: https://www.compoundchem.com/

These are the chemicals neurons use to communicate. If you have heard about neurons talking in electric signals, you may get confused now. Everything will make sense after this explanation.

So, the thing is: Neurons communicate via both electric and chemical signals. We know electric signals as “action potentials” and chemical ones as “neurotransmitters”. They work in tandem to produce the desired result.

How do neurons function?

In layman’s terms, the process involves the creation of action potential followed by the synthesis and release of neurotransmitters. Some ions influence this process; the most important of them is Calcium

1. Action potential

The resting action potential of the cell membrane of a neuron is about -65mV. Ions cause small and large changes in membrane potential. Oscillations under tens of millivolts are weak at carrying signals. To carry a signal requires a minimum potential difference of 100 mV (bringing the potential to about +20 mV). We call this big, drastic change ‘action potential’. Note: Fatty myelin sheaths over neurons increase transmission speed manifold.

2. Neurotransmitter Synthesis

The synaptic terminal of the axon houses many vesicles–tiny organelles–called “synaptic vesicles.” These contain neurotransmitters synthesized within the cell body. After synthesis, the neurotransmitters are packaged in the vesicles which have vesicular membranes.

Neurotransmitters include dopamine, GABA, serotonin, glutamate, glycine, histamine, and 100+ more. 

4. Neurotransmitter Release

Remember the action potential? Well, our two goals are to link that to the neurotransmitter release and prevent unintended release. So, how does a neuron accomplish this?

It’s simple. When the action potential reaches the synaptic terminal, ion channels open up in the plasma membrane. They make way for positively doubly charged Calcium ions (Ca2+). The Calcium ions, now surrounding the vesicles, cause vesicle-cell membrane fusion. It accomplishes this by binding to specific proteins, e.g. Synaptotagmin. This tears apart the vesicles, releasing the neurotransmitters. The vesicle must be within a few nanometers of the cell membrane to proceed with fusion.

What exactly causes the synaptic vesicle fusion? The SNARE Complex–a group of proteins (at least 24 in yeasts and 60+ in mammals)–mediates cell-vesicle or compartment-vesicle fusion. InterPro, SCOPe, TCDB and OPM superfamily are some SNARE complex protein symbols.

There is room for error during synaptic vesicle fusion. Clostridial toxins such as Botox (Botulinum toxin) can prevent neurotransmitter release by damaging the SNARE complex.

Botox is an example of a clostridial toxin. Yet, however counterintuitive, Botox can do good. A small dosage of locally administered Botox stops continuous automatic muscle contraction. Doctors now treat diseases like focal dystonia, neck spasms, hyperhidrosis and chronic migraines with Botox. One use of Botox may surprise you: Botox reduces wrinkles. Yeah; because neurotransmitter release causes them and Botox can stop that. 

So what happens next? After release, neurotransmitters spread out into the synoptic cleft; that’s the space between two adjacent neurons.

4. Signaling Message End

Pre-synaptic neuron is the cell sending the messages. We know the cell receiving it as post-synaptic.

A message can end in three ways:

Diffusion: The neurotransmitter particles spread out far enough from the active site of the post-synaptic cell.

Re-uptake: The pre-synaptic cell absorbs the neurotransmitter particles to recycle them.

Degradation: Enzymes in the way block neurotransmitters from reaching the desired site on the post-synaptic cell.

5. Message Reception

Multi-protein complexes on the post-synaptic neuron receive the signal. We call these “receptors.” Receptors are of two kinds: ‘ionotropic’ and ‘metabotropic’. 

The activation of Ionotropic receptors takes place by their corresponding neurotransmitter. When the neurotransmitter binds to the receptor, an ion pore opens up. This pore (or channel) facilitates Na+ and Cl intake and K+ discharge.

In contrast, metabotropic receptors are attached to a G-protein. We also call them GPCR (G-protein-Coupled Receptors). When a GPCR is activated, the G-protein performs some action. GPCRs have a varied function and are more inflexible.

Again, neurotransmitters are of distinct types. Some neurotransmitters have an excitatory effect (I.e. raise membrane potential) like glutamate. Others decrease membrane potential, like the inhibitory GABA. While excitatory neurotransmitters continue the signal chain, inhibitory transmitters break it. The receptor defines the nature of its neurotransmitter.

There can be issues with reception. For example, in Myasthenia Gravis, there’s a deduction in volume of acetylcholine receptors. This causes fewer acetylcholine molecules being affirmed. This causes a tremendous problem as acetylcholine is the protein responsible for motor function.

Neurons thus communicate and give rise to complex processes like memory formation. Here is a fun fact for you: Neurons can’t divide. Unlike other cells, neurons are incapable of this feat. In fact, it’s one of their unique characteristics. What we know as a brain tumor happens because of cancer of glial cells (which can divide) and other cell types; but never neurons.

I referenced the three major types of neurons in the introduction. They are: sensory neurons, motor neurons and interneurons.

And that was the grand finale of neuronal communication. The chain remains unbroken till reaching the signal’s intended destination; except if something interrupts it. This is how neurons talk to each other and pass messages for certain actions.

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