Myelin Sheath: Difference between revisions

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An action potential travels down a myelinated axon by [[Saltatory conduction|saltatory conduction]] which is where an action potential depolarises the axon enough to initiate the opening of the voltage gated sodium ion channels at the next node. This jumping of the action potential results in faster propagation and conservation of energy.  
An action potential travels down a myelinated axon by [[Saltatory conduction|saltatory conduction]] which is where an action potential depolarises the axon enough to initiate the opening of the voltage gated sodium ion channels at the next node. This jumping of the action potential results in faster propagation and conservation of energy.  


[[Multiple Sclerosis|Multiple Sclerosis]] is an [[Autoimmune disease|autoimmune disease]]<ref>http://www.mult-sclerosis.org/myelin.html</ref> where the myeline sheath is degenerated, causing random areas of inflammation called lesions<ref>http://www.mult-sclerosis.org/lesion.html</ref>. The glial cells can also be destroyed so regeneration cannot occur so the myelin sheath is replaced by scar tissue<ref>http://www.mult-sclerosis.org/lesion.html</ref>. The degenerated neurons cant transmit the action potential as quickly casusing symptoms such as loss of control of muscles and numbness.  
[[Multiple Sclerosis|Multiple Sclerosis]] is an [[Autoimmune disease|autoimmune disease]]<ref>http://www.mult-sclerosis.org/myelin.html</ref> where the myeline sheath is degenerated, causing random areas of inflammation called lesions<ref>http://www.mult-sclerosis.org/lesion.html</ref>. The glial cells can also be destroyed so regeneration cannot occur so the myelin sheath is replaced by scar tissue<ref>http://www.mult-sclerosis.org/lesion.html</ref>. The degenerated neurons can't transmit the action potential as quickly causing symptoms such as loss of control of muscles and numbness. Preventing brain atrophy may have important clinical implications affecting treatment decisions in the future. In recent years, research efforts have directed towards finding agents to modify the disease and reduce brain volume loss. Intravenous immunoglobulin (IVIg) may have some potential roles in this regard.<ref> Zare-Shahabadi, Rashidian, Sahraian, Rezaei (2015)(Potential role of immunoglobulin replacement therapy on MRI measures in multiple sclerosis: a systematic review.)


Invertebrates do not have myelinated neurons.  
Invertebrates do not have myelinated neurons.  

Revision as of 15:23, 22 October 2015

Many neurons in vertebrates are electrically insulated by a fatty layer called the myelin sheath produced by supportive cells called glial cells. There are different types of glial cells, oligodentrocytes surround neurons in the CNS and schwann cells surround periphral neurons[1], they produce the myelin sheath by the plasma membrane migrating around the neurons axon in a tight spiral. A single oligodentrocyte can myelinate up to 10-15 neurons whereas schwann cells only myelinate one[2]. Myelinated neurons are refered to as white matter as the myeline sheath is white[3].            

Between the glial cells are gaps called Nodes of Ranvier where voltage gated sodium ion channels are.

An action potential travels down a myelinated axon by saltatory conduction which is where an action potential depolarises the axon enough to initiate the opening of the voltage gated sodium ion channels at the next node. This jumping of the action potential results in faster propagation and conservation of energy.

Multiple Sclerosis is an autoimmune disease[4] where the myeline sheath is degenerated, causing random areas of inflammation called lesions[5]. The glial cells can also be destroyed so regeneration cannot occur so the myelin sheath is replaced by scar tissue[6]. The degenerated neurons can't transmit the action potential as quickly causing symptoms such as loss of control of muscles and numbness. Preventing brain atrophy may have important clinical implications affecting treatment decisions in the future. In recent years, research efforts have directed towards finding agents to modify the disease and reduce brain volume loss. Intravenous immunoglobulin (IVIg) may have some potential roles in this regard.Cite error: Closing </ref> missing for <ref> tag.

References