Axolemma
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Axolemma | |
---|---|
Details | |
Part of | Axon of a nerve |
System | Nervous system |
Identifiers | |
TH | H2.00.06.1.00003 |
FMA | 67246 |
Anatomical terminology |
The axolemma is the cell membrane of an axon. The similar term axoplasm refers to the cytoplasm of an axon. The axolemma is responsible for maintaining the membrane potential of the axon, and contains ion channels through which ions can flow rapidly.[1] When this occurs, the voltage inside the axon changes, and depolarization or hyperpolarization of the membrane can occur. Adequate depolarization can lead to an action potential, which travels down the axon in a self-propagating manner as more ion channels open due to stimulation by the influx of positive ions.[2] An unmyelinated axolemma has a high capacitance which imposes a restraint on the conduction speed.[citation needed]. The constricted axon segment is one of the few locations in which there is ten times more schwann cell membrane than axolemma, while other portions they have equal distributions.[3]
The axolemma is a bilipid membrane. Under standard electron microscope preparations the structure is approximately 8 nm thick. The axolemma is stabilized by subjacent part of the axoplasm where the axoplasmic cortex is formed of condensed cytoskeletal microtrabecular matrix.[4] The skeletal framework of this structure is formed by spectrum in a hexagonal or pentagonal arrangement on the inside of the cell membrane, as well as actin connected to the transmembrane. The metric cellular matrix is bound by transmembrane proteins, including the β1-integrin, to the cytoskeleton via the membrane skeleton.[5]
If the axolemma is damaged, it becomes unable to perform its vital role of maintaining the concentration gradient of ions inside and outside the cell. When ions move down their concentration gradient into the cell, they can cause a number of different cellular processes that may lead to cell damage or cell death.[citation needed]
Axolemma is involved in preventing the hyperexcitability of gray matter axons.[1]
References[]
- ^ Jump up to: a b Hamada, M. S.; Kole, M. H. P. (6 May 2015). "Myelin Loss and Axonal Ion Channel Adaptations Associated with Gray Matter Neuronal Hyperexcitability". Journal of Neuroscience. 35 (18): 7272–7286. doi:10.1523/JNEUROSCI.4747-14.2015. PMC 4420788. PMID 25948275.
- ^ Elaine N. Marieb and Katja Hoehn (2007). Human Anatomy & Physiology (7th ed.). Pearson. pp. 393–412. ISBN 978-0-8053-5909-1.
- ^ Stys, edited by Stephen G. Waxman, Jeffery D. Kocsis, Peter K. (1995). The axon : structure, function, and pathophysiology. New York: Oxford University Press. p. 39. ISBN 0195082931.CS1 maint: extra text: authors list (link)
- ^ Berthold, C.-H.; Fraher, John P.; King, R.H.M.; Rydmark, Martin (2005). "Microscopic Anatomy of the Peripheral Nervous System". Peripheral Neuropathy. pp. 35–91. doi:10.1016/B978-0-7216-9491-7.50006-5. ISBN 9780721694917.
- ^ Fitzpatrick, M. O.; Maxwell, W. L.; Graham, D. I. (1 March 1998). "The role of the axolemma in the initiation of traumatically induced axonal injury". Journal of Neurology, Neurosurgery & Psychiatry. 64 (3): 285–287. doi:10.1136/jnnp.64.3.285. PMC 2169978. PMID 9527135.
External links[]
- Histology image: 22802loa – Histology Learning System at Boston University
- Neurohistology
- Cell biology stubs