CASE: A 19 year old Caucasian female from Canton, Ohio, is taken to her doctor’s office one afternoon by a co-worker after she had experienced stroke-like symptoms. Per the co-worker: the patient was working at her day job at Amazon, lifting boxes and placing them on conveyor belts. She was lifting a small box of “Keeping Up With the Kardashians” memorabilia, when she experienced the sudden onset of weakness in her bilateral upper extremities. Her co-worker noticed her friend standing in place with her arms extended and, confused, rushed her to the infirmary at the factory, after which she was told to go to her doctor. After questioning, the patient did state that she has experienced intermittent, occasional weakness which usually worsened as the day progressed. Throughout the day, she notices that her eyelids become progressively more droopy over time but that as she rests, her strength improves. After gathering this history, her physician decides to test her for a disorder known as myasthenia gravis by testing for the presence of nicotinic acetylcholine receptor antibodies. Given a POSITIVE result on this testing, the patient was subsequently diagnosed with myasthenia gravis. Please address the following: What is the normal physiology of the neuromuscular junction?
CASE: A 19 year old Caucasian female from Canton, Ohio, is taken to her doctor’s office one afternoon by a co-worker after she had experienced stroke-like symptoms. Per the co-worker: the patient was working at her day job at Amazon, lifting boxes and placing them on conveyor belts. She was lifting a small box of “Keeping Up With the Kardashians” memorabilia, when she experienced the sudden onset of weakness in her bilateral upper extremities.
Her co-worker noticed her friend standing in place with her arms extended and, confused, rushed her to the infirmary at the factory, after which she was told to go to her doctor. After questioning, the patient did state that she has experienced intermittent, occasional weakness which usually worsened as the day progressed. Throughout the day, she notices that her eyelids become progressively more droopy over time but that as she rests, her strength improves.
After gathering this history, her physician decides to test her for a disorder known as myasthenia gravis by testing for the presence of nicotinic acetylcholine receptor antibodies. Given a POSITIVE result on this testing, the patient was subsequently diagnosed with myasthenia gravis.
Please address the following:
- What is the normal physiology of the neuromuscular junction?
Person C is a 19 years old female who experienced stroke-like symptoms during lifting boxes. The patient had previously experienced intermittent, occasional weakness that usually worsened through the day. As day progresses, her eyelids become gradually droopy. If she rests she feels better.
Neuromuscular junction is the chemical synapse that is formed when a motor neuron comes in contact with a muscle fiber. At the neuromuscular junction, the motor neuron transmits the signal to the muscle fiber for muscle contraction. The normal physiology of the neuromuscular junction results in the release of ACh with its subsequent binding with ACh receptors.
The events that lead to release of the neurotransmitter ACh from a motor neuron at the neuromuscular junction are as follows:
- Calcium entry at the synaptic knob: A nerve impulse is propagated down an axon, which is sent along with a motor neuron to the somatic nervous system. The voltage-gated Ca2+ channels are triggered by the nerve signal within the synaptic knob plasma membrane. In this condition within the synaptic knob plasma membrane, the calcium ion moves down to its concentration gradient from the interstitial fluid through synaptic knob open channels.
- Release of ACh from the synaptic knob: Propagation of nerve impulse is down the motor axon, which triggers the opening of other calcium channels. The calcium ions move into the synaptic knob and bind to a membrane protein exposed to synaptic vesicles. The binding of calcium ions to synaptic vesicles triggers the merging of the synaptic knob with synaptic vesicles, resulting in exocytosis of Ach from the vesicle.
- Binding at the motor endplate: The neurotransmitter ACh diffuses across the fluid-filled synaptic cleft. This leads to binding of the synaptic cleft with the ACh receptors inside the motor endplate. This leads to skeletal muscle fiber excitation.
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