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Acetylcholinesterase Nicotinic Acetylcholine Receptor Nicotinic Acetylcholine Receptor Voltage- dependent L-type calcium channel subunit alpha-1C Myosin light chain kinase Choline O- acetyltransferase Myosin LC-P Myosin light chain 3 N-type calcium channel Vesicular acetylcholine transporter High affinity choline transporter 1 Calmodulin-1 Myosin light chain phosphatase Ca+ Acetylcholine Pyridostigmine Na+ Pyridostigmine Ca+ Choline Choline Na+ Ca+ Ca+ Pyridostigmine Pyridostigmine Acetyl-CoA Choline CoA H2O Acetic acid Manganese Ca+ Calmodulin-1 Acetylcholine Acetylcholine Muscle Contraction Muscle Relaxation Magnesium Presynaptic Neuron Motor End Plate 2. An action potential arrives at the nerve terminal and stimulates the opening of the calcium channel, causing an influx of calcium ions 1. Acetylcholine is synthesized and stored in synaptic vesicles at the nerve terminal 3. Calcium ions stimulates the release of neurotransmitter acetylcholine into the synaptic cleft via exocytosis 4. Acetylcholine in the synaptic cleft activates nicotinic receptors on the post-synaptic membrane 7. Acetylcholine is broken down by acetylcholinesterase into choline and acetyl-coa 8. Choline is taken back up into the nerve terminal and recycled to create more acetylcholine Pyridostigmine inhibits acetylcholinesterase, preventing acetylcholine breakdown 5. The activated nicotinic receptor stimulates sodium ion influx, depolarizing the cell Vesicle Pyridostigmine is administered orally and diffuses into the bloodstream and travels to its target within the brain Sacroplasmic Reticulum 6. Depolarization causes a release of calcium from the sarcoplasmic reticulum. Calcium binds to calmodulin that in turn activates myosin light chain kinase. Once phosphorylated starts initiating muscle contraction Neuromuscular Junction Pyridostigmine inhibits choline-o-acetyltransferase, leading to accumulation of acetylcholine in the synaptic cleft.
ACHE Unknown Unknown CACNA1C MYLK2 CHAT MYL3 MYL3 CACNB1 SLC18A3 SLC5A7 CALM1 PPP1CB Calcium Acetylcholine Pyridostigmine Sodium Pyridostigmine Calcium Choline Choline Sodium Calcium Calcium Pyridostigmine Pyridostigmine Acetyl-CoA Choline Coenzyme A Water Acetic acid Calcium CALM1 Acetylcholine Acetylcholine Muscle Contraction Muscle Relaxation
ACHE CACNA1C MYLK2 CHAT MYL3 MYL3 CACNB1 SLC18A3 SLC5A7 CALM1 PPP1CB Ca+ ACh Regonol Na+ Regonol Ca+ Choline Choline Na+ Ca+ Ca+ Regonol Regonol Ac-CoA Choline CoA H2O Acoh Mn2+ Ca+ CALM1 ACh ACh Mus Con Mus Rel Mg2+ Presynaptic Neuron Motor End Plate 2. An action potential arrives at the nerve terminal and stimulates the opening of the calcium channel, causing an influx of calcium ions 1. Acetylcholine is synthesized and stored in synaptic vesicles at the nerve terminal 3. Calcium ions stimulates the release of neurotransmitter acetylcholine into the synaptic cleft via exocytosis 4. Acetylcholine in the synaptic cleft activates nicotinic receptors on the post-synaptic membrane 7. Acetylcholine is broken down by acetylcholinesterase into choline and acetyl-coa 8. Choline is taken back up into the nerve terminal and recycled to create more acetylcholine Pyridostigmine inhibits acetylcholinesterase, preventing acetylcholine breakdown 5. The activated nicotinic receptor stimulates sodium ion influx, depolarizing the cell Vesicle Pyridostigmine is administered orally and diffuses into the bloodstream and travels to its target within the brain Sacroplasmic Reticulum 6. Depolarization causes a release of calcium from the sarcoplasmic reticulum. Calcium binds to calmodulin that in turn activates myosin light chain kinase. Once phosphorylated starts initiating muscle contraction Neuromuscular Junction Pyridostigmine inhibits choline-o-acetyltransferase, leading to accumulation of acetylcholine in the synaptic cleft.
ACHE CACNA1C MYLK2 CHAT MYL3 MYL3 CACNB1 SLC18A3 SLC5A7 CALM1 PPP1CB Ca2+ ACh Regonol Na+ Regonol Ca2+ Choline Choline Na+ Ca2+ Ca2+ Regonol Regonol Ac-CoA Choline CoA H2O Acoh Ca2+ CALM1 ACh ACh Mus Con Mus Rel