Neuromuscular junction

From The School of Biomedical Sciences Wiki
(Difference between revisions)
Jump to: navigation, search
Line 1: Line 1:
A neuromuscular junction is a type of [[Synapse|synapse]], a gap between a motor [[Neurone|neurone]] and the [[Muscle end plate|muscle end plate]] known as the synaptic cleft which is approximately 50nm wide. At a neuromuscular junction an [[Action potential|action potential]] passes from the [[Presynaptic membrane|presynaptic membrane]] to the [[Postsynaptic membrane|postsynaptic membrane]], also known as the junctional folds present on the muscle end plate. This is to allow signal to pass from neurone to muscle end plate which will result in the relaxation or the contraction of the muscle.  
+
A neuromuscular junction is a type of [[Synapse|synapse]]; a gap between a motor [[Neurone|neurone]] and the [[Muscle end plate|muscle end plate]] known as the synaptic cleft which is approximately 50nm wide. At a neuromuscular junction an [[Action potential|action potential]] passes from the [[Presynaptic membrane|presynaptic membrane]] to the [[Postsynaptic membrane|postsynaptic membrane]], also known as the junctional folds present on the muscle end plate. This is to allow the signal to pass from the neurone to the muscle end plate, which will result in the relaxation or the contraction of the muscle.  
  
 
In order for this action potential to be passed on to the [[Postsynaptic membrane|postsynaptic membrane]] several steps occur:  
 
In order for this action potential to be passed on to the [[Postsynaptic membrane|postsynaptic membrane]] several steps occur:  
  
#An [[Action potential|action potential]] (generated at the axon hillox) travels down the axon by the saltatory effect to reach the [[Axon|axon]] terminal. This causes the [[Depolarisation|depolarisation]] of the presynaptic membrane which results in the opening of the voltage-gated calcium channels.  
+
#An [[Action potential|action potential]] (generated at the axon hillock) travels down the axon by saltatory conduction to reach the [[Axon|axon]] terminal. This causes the [[Depolarisation|depolarisation]] of the presynaptic membrane, which results in the opening of the voltage-gated calcium channels.  
#[[Calcium|Calcium]] [[Ions|ions]] move down their concentration gradient into the presynaptic membrane causing [[Vesicle|vesicles]] containing the [[Neurotransmitter|neurotransmitter]] [[Acetylcholine|acetylcholine]] (the most common [[Neurotransmitter|neurotransmitter]]) to fuse with the presynaptic membrane. Influx of calcium ions is an example of facilitated diffusion while release of the nerotransmitter is an example of exocitosis. At the neromuscular junction we have conversion of the electric signal into a chmical signal whereby acetylcholine acts as the signalling molecule.  
+
#[[Calcium|Calcium]] [[Ions|ions]] move throught the presynaptic membrane (down their concentration gradient) and into the axon. This causes [[Vesicle|vesicles]] that contain the [[Neurotransmitter|neurotransmitter]] [[Acetylcholine|acetylcholine]] (the most common [[Neurotransmitter|neurotransmitter]]) to fuse with the presynaptic membrane. This influx of calcium ions is an example of [[Facilitated_diffusion|facilitated diffusion ]]while the release of the nerotransmitter is an example of [[Exocytosis|exocytosis]]. At the neromuscular junction the electric signal is converted into a chemical signal whereby the acetylcholine acts as the signalling molecule.  
#The neurotransmitter [[Acetylcholine|acetylcholine]], then diffuses across the [[Synaptic cleft|synaptic cleft]] within less than 1 ms and binds to specific receptor [[Proteins|proteins]] on the postsynaptic membrance of the muscle end plate.  
+
#The neurotransmitter [[Acetylcholine|acetylcholine]] then diffuses across the [[Synaptic cleft|synaptic cleft]] (which is less than 1 ms in width) and binds to specific receptor [[Proteins|proteins]] on the postsynaptic membrance of the muscle end plate.  
#The receptor protein is in fact a ligand-gated sodium channel and hence opens upon reception of signal.  
+
#The receptor protein is a ligand-gated sodium channel which then opens upon reception of the signal.  
#[[Sodium|Sodium]] [[Ions|ions]] diffuse down their concentration gradient into the postsynaptic membrane, and potassium ions diffuse out of the postsynaptic membrane. This causes the depolarisation to be passed on to the muscle end plate, and the action potential continues.  
+
#The opening of the channel causes an influx of [[Sodium|Sodium]] [[Ions|ions]], which diffuse down their concentration gradient into the postsynaptic membrane. As well as this potassium ions also diffuse out of the postsynaptic membrane. This causes depolarisation within the the muscle end plate, and the action potential continues.  
#To close the [[Ligand-gated sodium channels|ligand-gated sodium channels]] and stop the depolarisation of the muscle end plate, an enzyme called [[Acetylcholinesterase|acetylcholinesterase]] binds to [[Acetylcholine|acetylcholine]] and breaks it down. It is broken down into choline and acetate.&nbsp;Choline is then taken up to be recycled by the presynaptic membrane.<br>
+
#To close the [[Ligand-gated sodium channels|ligand-gated sodium channels]] and stop the depolarisation of the muscle end plate, an enzyme called [[Acetylcholinesterase|acetylcholinesterase]] binds to [[Acetylcholine|acetylcholine]] and breaks it down into choline and acetate.&nbsp;Choline is then taken up to be recycled by the presynaptic membrane.<br>
  
The EPP on the post synaptic membrane reaches -15 mV. This value is half way between the equilibrium potentials of the sodium and potassium ions. Importantly -15 mV is not a full depolarisation but is greater than the threshold potential (-55mV) and hence can trigger an action potential within the junctional folds where [[Sodium_voltage-gated_ion_channels|voltage gated sodium channels]] exist. The action potential triggered in the membrane then lead to contraction of the [[muscle|muscles]]&nbsp;<ref>Alberts, Johnson, Lewis, Raff, Roberts, Walter; Molecular Biology of the cell, fifth edition; page 687-688, Garland Science</ref>&nbsp;<ref>Boyle and Senior, Biology, Collins Advanced Science, second edition, pages 354-357</ref>.  
+
The EPP (End Plate Potential) on the post synaptic membrane reaches -15 mV. This value is half way between the equilibrium potentials of the sodium and potassium ions. Importantly -15 mV is not a full depolarisation but is greater than the threshold potential (-55mV) and hence can trigger an action potential within the junctional folds where [[Sodium voltage-gated ion channels|voltage gated sodium channels]] exist. The action potential triggered in the membrane then lead to contraction of the [[Muscle|muscles]]&nbsp;<ref>Alberts, Johnson, Lewis, Raff, Roberts, Walter; Molecular Biology of the cell, fifth edition; page 687-688, Garland Science</ref>&nbsp;<ref>Boyle and Senior, Biology, Collins Advanced Science, second edition, pages 354-357</ref>.  
  
=== References ===
+
=== References ===
  
 
<references />
 
<references />
  
 
===  ===
 
===  ===

Revision as of 14:09, 23 October 2013

A neuromuscular junction is a type of synapse; a gap between a motor neurone and the muscle end plate known as the synaptic cleft which is approximately 50nm wide. At a neuromuscular junction an action potential passes from the presynaptic membrane to the postsynaptic membrane, also known as the junctional folds present on the muscle end plate. This is to allow the signal to pass from the neurone to the muscle end plate, which will result in the relaxation or the contraction of the muscle.

In order for this action potential to be passed on to the postsynaptic membrane several steps occur:

  1. An action potential (generated at the axon hillock) travels down the axon by saltatory conduction to reach the axon terminal. This causes the depolarisation of the presynaptic membrane, which results in the opening of the voltage-gated calcium channels.
  2. Calcium ions move throught the presynaptic membrane (down their concentration gradient) and into the axon. This causes vesicles that contain the neurotransmitter acetylcholine (the most common neurotransmitter) to fuse with the presynaptic membrane. This influx of calcium ions is an example of facilitated diffusion while the release of the nerotransmitter is an example of exocytosis. At the neromuscular junction the electric signal is converted into a chemical signal whereby the acetylcholine acts as the signalling molecule.
  3. The neurotransmitter acetylcholine then diffuses across the synaptic cleft (which is less than 1 ms in width) and binds to specific receptor proteins on the postsynaptic membrance of the muscle end plate.
  4. The receptor protein is a ligand-gated sodium channel which then opens upon reception of the signal.
  5. The opening of the channel causes an influx of Sodium ions, which diffuse down their concentration gradient into the postsynaptic membrane. As well as this potassium ions also diffuse out of the postsynaptic membrane. This causes depolarisation within the the muscle end plate, and the action potential continues.
  6. To close the ligand-gated sodium channels and stop the depolarisation of the muscle end plate, an enzyme called acetylcholinesterase binds to acetylcholine and breaks it down into choline and acetate. Choline is then taken up to be recycled by the presynaptic membrane.

The EPP (End Plate Potential) on the post synaptic membrane reaches -15 mV. This value is half way between the equilibrium potentials of the sodium and potassium ions. Importantly -15 mV is not a full depolarisation but is greater than the threshold potential (-55mV) and hence can trigger an action potential within the junctional folds where voltage gated sodium channels exist. The action potential triggered in the membrane then lead to contraction of the muscles [1] [2].

References

  1. Alberts, Johnson, Lewis, Raff, Roberts, Walter; Molecular Biology of the cell, fifth edition; page 687-688, Garland Science
  2. Boyle and Senior, Biology, Collins Advanced Science, second edition, pages 354-357

Personal tools
Namespaces
Variants
Actions
Navigation
Toolbox