We’re all familiar with the nervous system in mammals (particularly humans) and how the various impulses and responses are communicated through the intricate neural network stemming from the brain and spinal cord. But, what would we find if we had to closely examine a synapse? The axon terminal is a critical part of the nervous system, and we’ll investigate why below.

The axon terminal is an essential part of the neuron. The axon terminal is the “end-part” of the axon, which lies adjacent to a synapse, the gap between two consecutive neurons. Axon terminals play a fundamental role in facilitating intercellular communication through neurotransmitters.

The neuron is one of the most vital cells in the body. If nerve impulses are not effectively conducted through the body, the organism stands to suffer. The axon terminal plays a pivotal role in bridging the synapse. But how does it do this? Where exactly are axon terminals located? And what are some complications they experience?

An Axon Terminal’s Structure And LocationThe Purpose And Function Of An Axon TerminalComplications Of The Axon TerminalConclusion

An Axon Terminal’s Structure And Location

The Purpose And Function Of An Axon Terminal

Complications Of The Axon Terminal

Conclusion

The Definition Of A Axon Terminal

According to theFree Medical Dictionary, the axon terminal is the “ending of an axonwhich releasesneurotransmittersinto a synaptic space near another neuron, muscle, or gland cell.”

Another way to understand an axon terminal is itsetymology(where the name derives from).

The name“axon”is from theAncient Greek word(ἄξων) for “áxōn” or“axis.”

The“terminal”part of the name comes from theLatinword “terminalis,” which describes aboundary.“Terminalis” was derived from “terminus” (Latin), meaning“a limit, or an end.”

The Structure And Location Of Axon Terminals

Axon terminals occurat every synapsethroughout the body(human and others). Axon terminals arebutton-like(or club-like) structures at the end of an axon. They are oftenenlargedcompared to the rest of the axon. And are oftenbranched.

Axon terminals haveoutput receptors(synaptic terminals) on their ends which lie next to the synapse.

The axon (and therefore the axon terminal)forms part of theneuron(the nerve cell).

Neuronsoccur throughout the body and consist of:

The Physiological Makeup Of Axon Terminals

Synaptic vesicles, containing neurotransmitters, “float around” in the axon terminals until they areactivated. There aredifferent typesof vesicles located in the axon terminal.

A synaptic vesicle is arelatively small organelle(approximately 40nm). Due to the small size, synaptic vesicles can only accommodate alimited amount of proteins and phospholipids.

Although measurements are inconclusive, thereare an estimated10 000 moleculesof phospholipids in each vesicle and roughly200 proteins.

Some of theneurotransmitterswithin the synaptic vesicleinclude:

Axon terminalsfacilitate communication betweenthe axon of one neuron and the dendrites of otherneurons or effector cells(muscle and gland cells) across asynaptic gap.

Thepurposeof this synapse (connection gap) is totransfer “efferent”(outgoing)information(called action potentials and nerve impulses)“forward”through the axon of the presynaptic neuron into the postsynaptic neuron’s (or other cells) dendrites.

There aretwoprincipal types of synapses.

These signals carry agraded potential, which might not be strong enough to initiate the action potential needed for neurotransmitters.

Without theaxon terminaland its associated parts,neurons could not communicate.

Scientists believe that thesynaptic vesicles, located within the axon terminal,have the sole purposeof releasingneurotransmitters.

The exact “function” of many of thespecific vesicle proteinsis yet unknown (i.e., what specific proteins stimulate).

The table below examinessome synaptic vesicle proteinsand their functions.

Scientists divide theseproteins into two categories.

How The Axon Terminal Works

Anaction potentialis an eclectic chargethat alters the neuron’s membrane potential.Sodiummovingintothe cell whilepotassium moves outcreates the action potential. When not in use, a neuron has a “resting potential.”

Avoltage differencebetween theoutside and insideof a neuron’s membrane results in a charge. Whenneurotransmittersfrom the preceding neuron make contact, they initiate achangein the charge.

Once a graded oraction potential(but mostly action) moves into the neuron, ittriggers the neurontopermitaccessto free-floatingcalcium ions. The process behind the influx of calcium ions is theelectrical depolarizationof the membrane (at the synapse).

Thesecalcium ionstrigger thevesicles to fuseagainst the axon terminal’s membrane. These calcium ions also trigger the variousproteinswithin the (synaptic) vesicle toform fusion poresalong the axon terminal/vesicle membrane.

As the neurotransmitters move between neurons, theybind to the postsynaptic neuron’s receptors(located on the membranes of the dendrites). Once this neuron receives the“information,”it creates anaction potentialin theaxon hillock, which triggers the process.

The axon terminalallows the neuron to pass the informationon to subsequent neurons through neurotransmitters and electrochemical signals.

Axonal Transport Within The Neuron

Neurons are not equal in length. Those in the brain are conceivably shorter than those in the peripheries. In most neurons, the body(soma) is usually the same size. However, theaxon lengthis what differs. The axons that stretch from the spinal cord to the feet are oftenup to 3.3 feetlong.

Thenuclease in the soma(cell body) synthesizes most of the importantcell materials. Once synthesized, these materials mustmove throughoutthe neuron, including down the axon (until the axon terminal).

Any movement relating to the axon is referred to asaxonal transport. Important to note is that the movement ofcellular materialsis a“two-way”street. When materialsmove toward the axonterminal, it’s calledanterograde transport.

When materialsmove away from the axonterminal (toward the soma), it’s calledretrograde transport.

Trafficflows both ways simultaneouslyin the neuron. Within the axon,microtubulesprovide “highways” for cellular materials to move. The “horsepower” for movement comes frommotor proteins, which bind to the relevant material and move through the tubule.

Although vesicles, mitochondria, and other matter important to the neuron don’t travel through the tubule, the motor proteinsact like a train, carrying their load along the microtubule train tracks.

Kinesinis the motor protein that moves materialanterogradely, whilecytoplasmic dyneinmoves materialsretrogradely.

Some of theimportant materialswhich move from the soma to the axon terminal include:

Why Correct Functioning Of The Axon Terminal Is Essential

Withouta properly functioning axon terminal,nerve cells could not pass messagesthrough the body effectively, rendering the organism unable to function correctly.

Neurotransmitters areessential for various functions, like movement, metabolic activity, and hormone secretions.

In severe cases, aloss of functionalityin the axon terminal could lead toparalysis(i.e., muscles no longer function as they should),injury(sensory nerves do not convey the message swiftly enough), anddeath(either through injury or loss of critical function like breathing).

Microtubules position themselves in all directions within the soma. Inside the axon, the microtubule’spositively charged endpoints toward the axon terminal, while thenegatively charged endpoints towards the cell body.

Below we’ll investigate how theaxon terminal is negatively affected, including various diseases and injuries.

Toxins Bind To And Limit The Axon Terminal’s Function

Toxinsaffect neuromuscular interaction. In ahealthy, functional system, themotor neurons(axon terminals) make asynapsewith a skeletal muscle cell’smotor end plate.

As theaction potentialmoves into the presynaptic neuron, itstimulates the neuron’s membraneto permit calcium ions to enter the cell. As these ions enter, the synapticvesicles, which contain acetylcholine (a neurotransmitter),fuseto the axon terminal’s cell membrane.

Once fused, theneurotransmitters floodinto the synapse and bind to receptors in the muscle cell membrane (specifically nicotinic acetylcholine receptors).

The purpose and result of this process are that themuscle contacts.

However,variousproteinsand other molecules are involved in this process, which is susceptible to toxins. These toxins bind to the proteins on either side of the synaptic rift.

Once bound, thesetoxins reduce or preventthe neuron’s functioning, leading to muscleparalysis.

Inmedicine, doctors harness this binding trait of certain toxins torelax musclesfor diagnostic and research purposes.

Congenital Myasthenic Syndromes

When theneuromuscular proteins mutate, it often leads to various congenital myasthenic syndromes. These syndromes result inimpaired functionwithin the axon terminal and the receptor cells of the postsynaptic cell.

Theparts of the acetylcholine receptorsare the most frequently affected areas.

These mutations potentially lead tomuscle weaknessand, in rare cases,congenital myasthenic syndromes.

Thethree commonly occurring autoimmunedisorders affecting the neuromuscular junction are:

The Devastating Effects Of Trauma On The Axon Terminal

Trauma isanother reasonaxon terminals (and neurons)no longer workeffectively. For example, if an individual sustains ahead injury,the axons are usually damaged, and the individual is often left in avegetative state.

When anaxon tears, it can also lead toloss of consciousness, axon degeneration, and eventual nerve death. When axons experiencetrauma(crushing or severing), it leads toWallerian degeneration.

References

https://www.biologyonline.com/dictionary/axon-terminal

https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/axon-terminal

https://organismalbio.biosci.gatech.edu/chemical-and-electrical-signals/neurons/

https://study.com/learn/lesson/what-is-an-axon-terminal-function-types.html

https://medical-dictionary.thefreedictionary.com/axon+terminal

https://kids.frontiersin.org/articles/10.3389/frym.2020.00012

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