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Synap­tic Trans­mis­sion at the Neu­ro­mus­cu­lar Junction 1. An Action Poten­tial (AP) is con­ducted down the somatic motorneu­ron down to the synap­tic knob. 2. The rever­sal in elec­tri­cal polar­ity at the synap­tic knob causes an open­ing of “voltage-gated” Ca+2 chan­nels  (Volt­age gated cal­cium ion chan­nels open and allow cal­cium ions to flow inside due to the volt­age change).  Cal­cium ions are very impor­tant for the release of neu­ro­trans­mit­ters and secre­tion of hor­mones by endocrine cells. 3. Cal­cium flows into the synap­tic knob and it’s this influx that causes these vesi­cles to form and release/secrete neu­ro­trans­mit­ters.  In other words, the entry of Ca+ into the synap­tic knob causes the exo­cy­to­sis (secre­tion) of the nero­trans­mit­ter Acetyl­choline (ACh). 4.  The ACh dif­fuses across the synap­tic cleft and binds to “nico­tinic” ACh Recep­tor Site Pro­teins on the mem­brane of the Skele­tal Mus­cle Cell (Fiber).  The first chem­i­cal they dis­cov­ered that affects this recep­tor site, hap­pened to be nico­tine so that’s why it got the name, nico­tinic cholin­er­gic receptor. 5. Acti­va­tion of the ACh Recep­tor Sites causes an open­ing of “ligand-gated” Sodium Ion Chan­nels. 6. As sodium ions flow into the Skele­tal Mus­cle Cell, it depo­lar­izes to the thresh­old poten­tial, trig­ger­ing an Action Potential. 7. As the action poten­tial spreads along the cell, it causes the mus­cle cell to contract. 8. The ACh which is attached to the recep­tor site, is split into acetate and choline by acetyl­cholinesterase (ACHase), an enzyme of the skele­tal mus­cle cell membrane. 9. The “ligand-gated” sodium ion chan­nels close, per­mit­ting the skele­tal mus­cle cell to relax. 10. The acetate & choline are actively trans­ported back-up into the synap­tic knob (“Active Reup­take”) to be re-synthesized. Even­tu­ally, we’re going to talk about a neu­ro­trans­mit­ter in our brain called Sero­tonin.  There’s a class of med­i­cines called Selec­tive Sero­tonin Reup­take Inhibitors (SSRI).  This con­cept of reup­take will appear when we inves­ti­gate how these drugs works. » Ach attaches to an ACh recep­tor site -> Increased per­me­abil­ity to sodium, mean­ing the ligand-gated sodium ion chan­nels open -> Sodium rushes into mus­cle fiber -> Depo­lar­iza­tion (less neg­a­tive) -> Action Poten­tial -> Mus­cle Con­trac­tion.  Text­books call this depo­lar­iza­tion an End Plate Poten­tial (EPP).

Synap­tic Trans­mis­sion at the Neu­ro­mus­cu­lar Junction
 
1. An Action Poten­tial (AP) is con­ducted down the somatic motorneu­ron down to the synap­tic knob.
 
2. The rever­sal in elec­tri­cal polar­ity at the synap­tic knob causes an open­ing of “voltage-gated” Ca+2 chan­nels  (Volt­age gated cal­cium ion chan­nels open and allow cal­cium ions to flow inside due to the volt­age change).  Cal­cium ions are very impor­tant for the release of neu­ro­trans­mit­ters and secre­tion of hor­mones by endocrine cells.
 
3. Cal­cium flows into the synap­tic knob and it’s this influx that causes these vesi­cles to form and release/secrete neu­ro­trans­mit­ters.  In other words, the entry of Ca+ into the synap­tic knob causes the exo­cy­to­sis (secre­tion) of the nero­trans­mit­ter Acetyl­choline (ACh).
 
4.  The ACh dif­fuses across the synap­tic cleft and binds to “nico­tinic” ACh Recep­tor Site Pro­teins on the mem­brane of the Skele­tal Mus­cle Cell (Fiber).  The first chem­i­cal they dis­cov­ered that affects this recep­tor site, hap­pened to be nico­tine so that’s why it got the name, nico­tinic cholin­er­gic receptor.
 
5. Acti­va­tion of the ACh Recep­tor Sites causes an open­ing of “ligand-gated” Sodium Ion Chan­nels.
 
6. As sodium ions flow into the Skele­tal Mus­cle Cell, it depo­lar­izes to the thresh­old poten­tial, trig­ger­ing an Action Potential.
 
7. As the action poten­tial spreads along the cell, it causes the mus­cle cell to contract.
 
8. The ACh which is attached to the recep­tor site, is split into acetate and choline by acetyl­cholinesterase (ACHase), an enzyme of the skele­tal mus­cle cell membrane.
 
9. The “ligand-gated” sodium ion chan­nels close, per­mit­ting the skele­tal mus­cle cell to relax.
 
10. The acetate & choline are actively trans­ported back-up into the synap­tic knob (“Active Reup­take”) to be re-synthesized.
 
Even­tu­ally, we’re going to talk about a neu­ro­trans­mit­ter in our brain called Sero­tonin.  There’s a class of med­i­cines called Selec­tive Sero­tonin Reup­take Inhibitors (SSRI).  This con­cept of reup­take will appear when we inves­ti­gate how these drugs works.
 
» Ach attaches to an ACh recep­tor site -> Increased per­me­abil­ity to sodium, mean­ing the ligand-gated sodium ion chan­nels open -> Sodium rushes into mus­cle fiber -> Depo­lar­iza­tion (less neg­a­tive) -> Action Poten­tial -> Mus­cle Con­trac­tion.  Text­books call this depo­lar­iza­tion an End Plate Poten­tial (EPP).

Source: antranik.org
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