# Axoplasm

> Mediated Wiki article. Canonical URL: https://mediated.wiki/source/Axoplasm
> Markdown URL: https://mediated.wiki/source/Axoplasm.md
> Source: https://en.wikipedia.org/wiki/Axoplasm
> Source revision: 1321346610
> License: Creative Commons Attribution-ShareAlike 4.0 International (https://creativecommons.org/licenses/by-sa/4.0/)

Cytoplasm found within the axon of a neuron

Axoplasm Details Part of Axon of a nerve System Nervous system Identifiers Latin axoplasma TH H2.00.06.1.00019 Anatomical terminology [edit on Wikidata]

**Axoplasm** is the [cytoplasm](/source/Cytoplasm) within the [axon](/source/Axon) of a [neuron](/source/Neuron) (nerve cell). For some neuronal types this can be more than 99% of the total cytoplasm.[1]

Axoplasm has a different composition of [organelles](/source/Organelle) and other materials than that found in the neuron's [cell](/source/Cell_(biology)) body ([soma](/source/Soma_(cell_body))) or dendrites. In [axonal transport](/source/Axonal_transport) (also known as axoplasmic transport) materials are carried through the axoplasm to or from the soma.

## Structure

Axoplasm is composed of various organelles and cytoskeletal elements. The axoplasm contains a high concentration of elongated [mitochondria](/source/Mitochondria), [microfilaments](/source/Microfilament), and [microtubules](/source/Microtubules).[2] Axoplasm lacks much of the cellular machinery ([ribosomes](/source/Ribosomes) and [nucleus](/source/Cell_nucleus)) required to [transcribe](/source/Transcription_(genetics)) and translate complex [proteins](/source/Proteins). As a result, most enzymes and large proteins are transported from the soma through the axoplasm. Axonal transport occurs either by fast or slow transport. Fast transport involves vesicular contents (like organelles) being moved along microtubules by [motor proteins](/source/Motor_proteins) at a rate of 50–400mm per day.[3] Slow axoplasmic transport involves the movement of cytosolic soluble proteins and cytoskeletal elements at a much slower rate of 0.02-0.1mm/d. The precise mechanism of slow axonal transport remains unknown but recent studies have proposed that it may function by means of transient association with the fast axonal transport [vesicles](/source/Vesicle_(biology_and_chemistry)).[4] Though axonal transport is responsible for most organelles and complex proteins present in the axoplasm, recent studies have shown that some translation does occur in axoplasm. This axoplasmic translation is possible due to the presence of localized translationally silent [mRNA](/source/MRNA) and ribonuclear [protein complexes](/source/Protein_complexes).[5]

## Function

### Damage detection and regeneration

Axoplasm contains both the mRNA and ribonuclearprotein required for axonal protein synthesis. Axonal protein synthesis has been shown to be integral in both [neural regeneration](/source/Neural_regeneration) and in localized responses to axon damage.[5] When an axon is damaged, both axonal translation and retrograde axonal transport are required to propagate a signal to the soma that the cell is damaged.[5]

## History

Axoplasm was not a main focus for neurological research until after many years of learning of the functions and properties of [squid giant axons](/source/Squid_giant_axon). Axons in general were very difficult to study due to their narrow structure and in close proximity to [glial cells](/source/Glial_cells).[6] To solve this problem squid axons were used as an animal model due to the relatively vast sized axons compared to humans or other mammals.[7] These axons were mainly studied to understand action potential, and axoplasm was soon understood to be important in [membrane potential](/source/Membrane_potential).[8] The axoplasm was at first just thought to be very similar to cytoplasm, but axoplasm plays an important role in transference of nutrients and electrical potential that is generated by neurons.[9]

It actually proves quite difficult to isolate axons from the [myelin](/source/Myelin) that surrounds it,[10] so the squid giant axon is the focus for many studies that touch on axoplasm. As more knowledge formed from studying the signalling that occurs in neurons, transfer of nutrients and materials became an important topic to research. The mechanisms for the proliferation and sustained electrical potentials were affected by the fast axonal transport system. The fast axonal transport system uses the axoplasm for movement, and contains many non-conductive molecules that change the rate of these electrical potentials across the axon,[11] but the opposite influence does not occur. The fast axonal transport system is able to function without an axolemma, implying that the electrical potential does not influence the transport of materials through the axon.[12] This understanding of the relationship of axoplasm regarding transport and electrical potential is critical in the understanding of the overall brain functions.

With this knowledge, axoplasm has become a model for studying varying cell signaling and functions for the research of neurological diseases like [Alzheimer's](/source/Alzheimer's),[13] and [Huntington's](/source/Huntington's).[14] Fast axonal transport is a crucial mechanism when examining these diseases and determining how a lack of materials and nutrients can influence the progression of neurological disorders.

## References

1. **[^](#cite_ref-1)** Sabry, J.; O’Connor, T. P.; Kirschner, M. W. (1995). ["Axonal Transport of Tubulin in Ti1 Pioneer Neurons in Situ"](https://doi.org/10.1016%2F0896-6273%2895%2990271-6). *Neuron*. **14** (6): 1247–1256. [doi](/source/Doi_(identifier)):[10.1016/0896-6273(95)90271-6](https://doi.org/10.1016%2F0896-6273%2895%2990271-6). [PMID](/source/PMID_(identifier)) [7541635](https://pubmed.ncbi.nlm.nih.gov/7541635).

1. **[^](#cite_ref-2)** Hammond, C. (2015). *Cellular and Molecular Neurophysiology* (4th ed.). Academic Press. p. 433. [ASIN](/source/ASIN_(identifier)) [B00XV3J0UE](https://www.amazon.com/dp/B00XV3J0UE).

1. **[^](#cite_ref-3)** Brady, S. T. (1993). *Axonal dynamics and regeneration*. New York: Raven Press. pp. 7–36.{{[cite book](https://en.wikipedia.org/wiki/Template:Cite_book)}}: CS1 maint: publisher location ([link](https://en.wikipedia.org/wiki/Category:CS1_maint:_publisher_location))

1. **[^](#cite_ref-4)** Young, Tang (2013). ["Fast Vesicle Transport Is Required for the Slow Axonal Transport of Synapsin"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3782618). *Neuroscience*. **33** (39): 15362–15375. [doi](/source/Doi_(identifier)):[10.1523/jneurosci.1148-13.2013](https://doi.org/10.1523%2Fjneurosci.1148-13.2013). [PMC](/source/PMC_(identifier)) [3782618](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3782618). [PMID](/source/PMID_(identifier)) [24068803](https://pubmed.ncbi.nlm.nih.gov/24068803).

1. ^ [***a***](#cite_ref-Piper_5-0) [***b***](#cite_ref-Piper_5-1) [***c***](#cite_ref-Piper_5-2) Piper, M; Holt, C. (2004). ["RNA Translation in Axons"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682640). *Annual Review of Cell and Developmental Biology*. **20**: 505–523. [doi](/source/Doi_(identifier)):[10.1146/annurev.cellbio.20.010403.111746](https://doi.org/10.1146%2Fannurev.cellbio.20.010403.111746). [PMC](/source/PMC_(identifier)) [3682640](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3682640). [PMID](/source/PMID_(identifier)) [15473850](https://pubmed.ncbi.nlm.nih.gov/15473850).

1. **[^](#cite_ref-6)** Gilbert, D. (1975). ["Axoplasm chemical composition in Myxicola and solubility properties of its structural proteins"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1348544). *The Journal of Physiology*. **253** (1): 303–319. [doi](/source/Doi_(identifier)):[10.1113/jphysiol.1975.sp011191](https://doi.org/10.1113%2Fjphysiol.1975.sp011191). [PMC](/source/PMC_(identifier)) [1348544](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1348544). [PMID](/source/PMID_(identifier)) [1260](https://pubmed.ncbi.nlm.nih.gov/1260).

1. **[^](#cite_ref-7)** Young, J. (1977). *What squids and octopuses tell us about brains and memories* (1 ed.). American Museum of Natural History.

1. **[^](#cite_ref-8)** Steinbach, H.; Spiegelman, S. (1943). "The sodium and potassium balance in squid nerve axoplasm". *Journal of Cellular and Comparative Physiology*. **22** (2): 187–196. [doi](/source/Doi_(identifier)):[10.1002/jcp.1030220209](https://doi.org/10.1002%2Fjcp.1030220209).

1. **[^](#cite_ref-9)** Bloom, G. (1993). ["GTP gamma S inhibits organelle transport along axonal microtubules"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119514). *The Journal of Cell Biology*. **120** (2): 467–476. [doi](/source/Doi_(identifier)):[10.1083/jcb.120.2.467](https://doi.org/10.1083%2Fjcb.120.2.467). [PMC](/source/PMC_(identifier)) [2119514](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2119514). [PMID](/source/PMID_(identifier)) [7678421](https://pubmed.ncbi.nlm.nih.gov/7678421).

1. **[^](#cite_ref-10)** DeVries, G.; Norton, W.; Raine, C. (1972). "Axons: isolation from mammalian central nervous system". *Science*. **175** (4028): 1370–1372. [Bibcode](/source/Bibcode_(identifier)):[1972Sci...175.1370D](https://ui.adsabs.harvard.edu/abs/1972Sci...175.1370D). [doi](/source/Doi_(identifier)):[10.1126/science.175.4028.1370](https://doi.org/10.1126%2Fscience.175.4028.1370). [PMID](/source/PMID_(identifier)) [4551023](https://pubmed.ncbi.nlm.nih.gov/4551023). [S2CID](/source/S2CID_(identifier)) [30934150](https://api.semanticscholar.org/CorpusID:30934150).

1. **[^](#cite_ref-11)** Brady, S. (1985). "A novel brain ATPase with properties expected for the fast axonal transport motor". *Nature*. **317** (6032): 73–75. [Bibcode](/source/Bibcode_(identifier)):[1985Natur.317...73B](https://ui.adsabs.harvard.edu/abs/1985Natur.317...73B). [doi](/source/Doi_(identifier)):[10.1038/317073a0](https://doi.org/10.1038%2F317073a0). [PMID](/source/PMID_(identifier)) [2412134](https://pubmed.ncbi.nlm.nih.gov/2412134). [S2CID](/source/S2CID_(identifier)) [4327023](https://api.semanticscholar.org/CorpusID:4327023).

1. **[^](#cite_ref-12)** Brady, S.; Lasek, R.; Allen, R. (1982). "Fast axonal transport in extruded axoplasm from squid giant axon". *Science*. **218** (4577): 1129–1131. [Bibcode](/source/Bibcode_(identifier)):[1982Sci...218.1129B](https://ui.adsabs.harvard.edu/abs/1982Sci...218.1129B). [doi](/source/Doi_(identifier)):[10.1126/science.6183745](https://doi.org/10.1126%2Fscience.6183745). [PMID](/source/PMID_(identifier)) [6183745](https://pubmed.ncbi.nlm.nih.gov/6183745).

1. **[^](#cite_ref-13)** Kanaan, N.; Morfini, G.; LaPointe, N.; Pigino, G.; Patterson, K.; Song, Y.; Andreadis, A.; Fu, Y.; Brady, S.; Binder, L. (2011). ["Pathogenic forms of tau inhibit kinesin-dependent axonal transport through a mechanism involving activation of axonal phosphotransferases"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391724). *Neuroscience*. **31** (27): 9858–9868. [doi](/source/Doi_(identifier)):[10.1523/jneurosci.0560-11.2011](https://doi.org/10.1523%2Fjneurosci.0560-11.2011). [PMC](/source/PMC_(identifier)) [3391724](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3391724). [PMID](/source/PMID_(identifier)) [21734277](https://pubmed.ncbi.nlm.nih.gov/21734277).

1. **[^](#cite_ref-14)** Morfini, G.; You, Y.; Pollema, S.; Kaminska, A.; Liu, K.; Yoshioka, K.; Björkblom, B.; Coffey, E.; Bagnato, C.; Han, D. (2009). ["Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin"](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739046). *Nature Neuroscience*. **12** (7): 864–871. [doi](/source/Doi_(identifier)):[10.1038/nn.2346](https://doi.org/10.1038%2Fnn.2346). [PMC](/source/PMC_(identifier)) [2739046](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739046). [PMID](/source/PMID_(identifier)) [19525941](https://pubmed.ncbi.nlm.nih.gov/19525941).

v t e Nervous tissue CNS Tissue Types Grey matter White matter Projection fibers Association fiber Commissural fiber Lemniscus Nerve tract Decussation Neuropil Meninges Cell Types Neuronal Pyramidal Purkinje Granule Von Economo Medium spiny Interneuron Glial Astrocyte Ependymal cells Tanycyte Oligodendrocyte progenitor cell Oligodendrocyte Microglia PNS General Dorsal Root Ganglion Ramus Ventral Root Ramus Ramus communicans Gray White Autonomic ganglion (Preganglionic nerve fibers Postganglionic nerve fibers) Nerve fascicle Funiculus Connective tissues Epineurium Perineurium Endoneurium Neuroglia Myelination: Schwann cell Neurilemma Myelin incisure Node of Ranvier Internodal segment Satellite glial cell Neurons/ nerve fibers Parts Soma Axon hillock Axon Telodendron Axon terminals Axoplasm Axolemma Neurofibril/neurofilament Dendrite Nissl body Dendritic spine Apical dendrite/Basal dendrite Types Bipolar Unipolar Pseudounipolar Multipolar Interneuron Renshaw Afferent nerve fiber/ Sensory neuron GSA GVA SSA SVA fibers Ia or Aα Ib or Golgi or Aα II or Aβ and Aγ III or Aδ or fast pain IV or C or slow pain Efferent nerve fiber/ Motor neuron GSE GVE SVE Upper motor neuron Lower motor neuron α motorneuron β motorneuron γ motorneuron Termination Synapse Electrical synapse/Gap junction Chemical synapse Synaptic vesicle Active zone Postsynaptic density Autapse Ribbon synapse Neuromuscular junction Sensory receptors Meissner's corpuscle Merkel nerve ending Pacinian corpuscle Ruffini ending Muscle spindle Free nerve ending Nociceptor Olfactory receptor neuron Photoreceptor cell Hair cell Taste receptor

---
Adapted from the Wikipedia article [Axoplasm](https://en.wikipedia.org/wiki/Axoplasm) by Wikipedia contributors ([contributor history](https://en.wikipedia.org/wiki/Axoplasm?action=history)). Available under [Creative Commons Attribution-ShareAlike 4.0 International](https://creativecommons.org/licenses/by-sa/4.0/). Changes may have been made.