January 1st, 2012
medicaljourney
These are images taken with an electron-micrograph of a neuromuscular junction of a mouse. Image A is the NMJ of a normal mouse. Image B is the NMJ of a mouse with myasthenia gravis (chemically induced for experimental purposes). The asterisk in each image is the nerve terminal. The dark round spots in each nerve terminal are the synaptic vesicles. In Image B, the mouse with myasthenia gravis, within the synaptic cleft there is a loss of synaptic folds, as well as “globular material” which represents NMJ folds that have been degenerated.[1]
Focusing specifically on acquired autoimmune myasthenia gravis, we find that most often, antibodies at the post-synaptic NMJ block ACh receptors, effectively inhibiting the effects of ACh on nicotinic acetylcholine receptors (nAChR). In some individuals the antibodies prevent ACh from binding to receptors and in other individuals, the antibodies destroy the receptors completely, generally by inducing the muscle cell to remove the receptors via endocytosis.[2]
When antibodies attack acetylcholine receptors, they are effectively attacking the endplate membrane. They do this by “fixing complement”[3] which results in destruction of Na+ channels and acetylcholine receptors from the endplate. The loss of functioning Na+ channels from the post-synaptic membrane/endplate in individuals suffering from MG can negatively impact neuromuscular transmission by increasing the threshold for muscle fiber spike generation, which decreases the size of the safety factor for NMJ transmission.[4]

[1] Kaminski, Henry J. Myasthenia Gravis and Related Disorders. New York: Humana, 2009. Print. Page 3


[2] Patrick, J., and J. Lindstrom. “Autoimmune Response to Acetylcholine Receptor.” Science 180.4088 (1973): 871-72. Print.


[3] Complement is a cascade of ~ 20 serum glycoproteins, the interaction of which functions in immunity and inflammation, including vasodilation, lysis of specific cells, and phagocyte activity.


[4] Meriggiolo, Matthew N., James F. Howard, and Thomas Michel. Harper. Neuromuscular Junction Disorders: Diagnosis and Treatment. New York: Marcel Dekker, 2003. Print. Pages 47-48

These are images taken with an electron-micrograph of a neuromuscular junction of a mouse. Image A is the NMJ of a normal mouse. Image B is the NMJ of a mouse with myasthenia gravis (chemically induced for experimental purposes). The asterisk in each image is the nerve terminal. The dark round spots in each nerve terminal are the synaptic vesicles. In Image B, the mouse with myasthenia gravis, within the synaptic cleft there is a loss of synaptic folds, as well as “globular material” which represents NMJ folds that have been degenerated.[1]

Focusing specifically on acquired autoimmune myasthenia gravis, we find that most often, antibodies at the post-synaptic NMJ block ACh receptors, effectively inhibiting the effects of ACh on nicotinic acetylcholine receptors (nAChR). In some individuals the antibodies prevent ACh from binding to receptors and in other individuals, the antibodies destroy the receptors completely, generally by inducing the muscle cell to remove the receptors via endocytosis.[2]

When antibodies attack acetylcholine receptors, they are effectively attacking the endplate membrane. They do this by “fixing complement”[3] which results in destruction of Na+ channels and acetylcholine receptors from the endplate. The loss of functioning Na+ channels from the post-synaptic membrane/endplate in individuals suffering from MG can negatively impact neuromuscular transmission by increasing the threshold for muscle fiber spike generation, which decreases the size of the safety factor for NMJ transmission.[4]


[1] Kaminski, Henry J. Myasthenia Gravis and Related Disorders. New York: Humana, 2009. Print. Page 3

[2] Patrick, J., and J. Lindstrom. “Autoimmune Response to Acetylcholine Receptor.” Science 180.4088 (1973): 871-72. Print.

[3] Complement is a cascade of ~ 20 serum glycoproteins, the interaction of which functions in immunity and inflammation, including vasodilation, lysis of specific cells, and phagocyte activity.

[4] Meriggiolo, Matthew N., James F. Howard, and Thomas Michel. Harper. Neuromuscular Junction Disorders: Diagnosis and Treatment. New York: Marcel Dekker, 2003. Print. Pages 47-48

  1. livingwithmyasthenia reblogged this from medicaljourney and added:
    These are images taken with an electron-micrograph of a neuromuscular junction of a mouse. Image A is the NMJ of a...
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I am a pre-medical postbaccalaureate student. This blog chronicles my journey through my pre-med program and beyond.

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