Editing Axoplasm (section)

==History==

Axoplasm was not a main focus for neurological research until after many years of learning of the functions and properties of [[squid giant axon]]s. Axons in general were very difficult to study due to their narrow structure and in close proximity to [[glial cells]].<ref>{{cite journal |last=Gilbert |first=D. |year=1975 |title=Axoplasm chemical composition in Myxicola and solubility properties of its structural proteins |journal=The Journal of Physiology |volume=253 |issue=1 |pages=303–319 |doi=10.1113/jphysiol.1975.sp011191|pmid=1260 |pmc=1348544 }}</ref> 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.<ref>{{cite book |last=Young |first=J. |year=1977 |title=What squids and octopuses tell us about brains and memories. |publisher= American Museum of Natural History. |edition=1}}</ref> These axons were mainly studied to understand action potential, and axoplasm was soon understood to be important in [[membrane potential]].<ref>{{cite journal |last1=Steinbach |first1=H. |last2=Spiegelman|first2=S. |year=1943 |title=The sodium and potassium balance in squid nerve axoplasm |journal= Journal of Cellular and Comparative Physiology|volume=22 |issue=2 |pages=187–196 |doi=10.1002/jcp.1030220209}}</ref> 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.<ref>{{cite journal |last=Bloom |first=G. |year=1993 |title=GTP gamma S inhibits organelle transport along axonal microtubules. |journal=  The Journal of Cell Biology|volume=120 |issue=2 |pages=467–476 |doi=10.1083/jcb.120.2.467|pmid=7678421 |pmc=2119514 }}</ref>

It actually proves quite difficult to isolate axons from the [[myelin]] that surrounds it,<ref>{{cite journal |last1=DeVries |first1=G. |last2=Norton|first2=W. |last3=Raine|first3=C.| year=1972 |title=Axons: isolation from mammalian central nervous system. |journal=Science |volume=175 |issue=4028 |pages=1370–1372 |doi=10.1126/science.175.4028.1370|pmid=4551023 |bibcode=1972Sci...175.1370D |s2cid=30934150 }}</ref> 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,<ref>{{cite journal |last=Brady |first=S.| year=1985 |title=A novel brain ATPase with properties expected for the fast axonal transport motor. |journal=Nature |volume=317 |issue=6032|pages=73–75 |doi=10.1038/317073a0|pmid=2412134|bibcode=1985Natur.317...73B|s2cid=4327023}}</ref> 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.<ref>{{cite journal |last1=Brady |first1=S.| last2=Lasek|first2=R. |last3=Allen|first3=R.|year=1982 |title=Fast axonal transport in extruded axoplasm from squid giant axon. |journal=Science |volume=218 |issue=4577|pages=1129–1131 |doi=10.1126/science.6183745|pmid=6183745|bibcode=1982Sci...218.1129B}}</ref> 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]],<ref>{{cite journal |last1=Kanaan |first1=N.| last2=Morfini|first2=G. |last3=LaPointe|first3=N. |last4=Pigino|first4=G. |last5=Patterson|first5=K. |last6=Song|first6=Y.|last7=Andreadis |first7=A.|last8=Fu |first8=Y.|last9=Brady|first9=S.|last10=Binder|first10=L.|year=2011 |title=Pathogenic forms of tau inhibit kinesin-dependent axonal transport through a mechanism involving activation of axonal phosphotransferases. |journal=Neuroscience |volume=31 |issue=27|pages=9858–9868 |doi=10.1523/jneurosci.0560-11.2011|pmid=21734277|pmc=3391724}}</ref> and [[Huntington's]].<ref>{{cite journal| last1=Morfini|first1=G. |last2=You|first2=Y. |last3=Pollema |first3=S. |last4=Kaminska |first4=A. |last5=Liu |first5=K. |last6=Yoshioka |first6=K. |last7=Björkblom |first7=B. |last8=Coffey |first8=E. |last9=Bagnato |first9=C. |last10=Han |first10=D. |year=2009 |title= Pathogenic huntingtin inhibits fast axonal transport by activating JNK3 and phosphorylating kinesin. |journal= Nature Neuroscience |volume=12 |issue=7 |pages=864–871 |doi=10.1038/nn.2346|pmid=19525941 |pmc=2739046 }}</ref> 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.