Neuromuscular junction and motor unit

30,523views

Neuromuscular junction and motor unit

AW3

AW3

Anatomy clinical correlates: Wrist and hand
Joint pain: Clinical
Osteoarthritis
Rheumatoid arthritis
Rheumatoid arthritis: Clinical
Rheumatoid arthritis and osteoarthritis: Pathology review
Septic arthritis
Reactive arthritis
Gout
Gout and pseudogout: Pathology review
Antigout medications
Non-steroidal anti-inflammatory drugs
Meniscus tear
Spinal disc herniation
Degenerative disc disease
Cauda equina syndrome
Lower back pain: Clinical
Sciatica
Bowel obstruction: Clinical
Gastrointestinal bleeding: Clinical
Gastrointestinal bleeding: Pathology review
Body fluid compartments
Movement of water between body compartments
Diverticulosis and diverticulitis
Diverticular disease: Pathology review
Diverticular disease: Clinical
Ischemic colitis
Microscopic colitis
Inflammatory bowel disease: Pathology review
Ulcerative colitis
Inflammatory bowel disease: Clinical
Irritable bowel syndrome
Portal hypertension
Cirrhosis
Cirrhosis: Clinical
Cirrhosis: Pathology review
Fitz-Hugh-Curtis syndrome
Celiac disease
Gastritis
Helicobacter pylori
GERD, peptic ulcers, gastritis, and stomach cancer: Pathology review
Barrett esophagus
Esophagus histology
Metaplasia and dysplasia
Anatomy of the breast
Anatomy clinical correlates: Breast
Mastitis
Benign breast conditions: Pathology review
Phyllodes tumor
Paget disease of the breast
Fibrocystic breast changes
Breast cancer
Breast cancer: Clinical
Breast cancer: Pathology review
Colorectal polyps
Oncogenes and tumor suppressor genes
Familial adenomatous polyposis
Pleural effusion
Pleural effusion: Clinical
Pleural effusion, pneumothorax, hemothorax and atelectasis: Pathology review
Puberty and Tanner staging
Prolactinoma
Neuromuscular blockers
Neuromuscular junction and motor unit
Pharmacodynamics: Agonist, partial agonist and antagonist
Anatomy of the hip joint
Sarcoidosis

Flashcards

Neuromuscular junction and motor unit

0 of 11 complete

Questions

USMLE® Step 1 style questions USMLE

0 of 1 complete

A study is conducted on a peripheral neuromuscular disease. In the study, the disease was found to occur secondary to autoimmune destruction of neuromuscular junction motor end-plate receptors. Which of the following is true regarding the type of these receptors and their associated signaling molecule?  

Transcript

Watch video only

In order for a skeletal muscle to contract, your brain sends a signal, in the form of an action potential in an upper motor neuron.

The upper motor neuron is part of the cerebral cortex, and it activates a lower motor neuron, which is located in the anterior horn of the spinal cord.

From here, the action potential is sent through an axon down to its ending branches, called axon terminals, to muscle fibers which they innervate.

The place where an axon terminal meets the muscle fiber is the neuromuscular junction.

The neuromuscular junction has three main parts: a presynaptic membrane, which is the membrane of an axon terminal; a postsynaptic membrane, which is the membrane of a skeletal muscle fiber and is also called a motor end-plate; and a synaptic cleft, which is the gap between the presynaptic and postsynaptic membrane.

When an action potential reaches the axon terminal, it stimulates voltage-gated calcium channels in the membrane to open and extracellular calcium ions flow into the lower motor neuron.

Inside the axon terminal are synaptic vesicles that contain neurotransmitters called acetylcholine.

The calcium that enters the axon terminal binds to the vesicles, which allows them to fuse with the cell membrane of the axon terminal, releasing the acetylcholine into the synaptic cleft.

The acetylcholine then diffuses over to the motor end plate on the muscle fiber - and because it’s a short distance, that diffusion happens really quickly.

Here, two acetylcholine molecules will bind to one ligand-gated ion channel, also called nicotinic receptor.

When that happens, these ligand-gated ion channels, which are selective for positively charged ions, open up.

When they open, lots of sodium ions rush into the skeletal muscle fiber, and a few potassium ions leak out of the cell.

But overall there’s an increase in positive charge on the inside of the muscle fiber and therefore on the inside of the membrane, relative to the outside of the membrane - and this is called depolarization.

This local depolarization on the postsynaptic membrane is called an end-plate potential and it makes the resting potential of the cell membrane which is usually around -100mV, more positive, or in this case, less negative.

The local depolarization causes the cell membrane’s resting potential to rise up to about -60mV, and that’s the threshold for voltage gated sodium ion channels.

Key Takeaways

The neuromuscular junction is a site where a motor neuron meets a skeletal muscle fiber. It is where a nerve impulse is transmitted from a motor neuron to a muscle fiber. A neuromuscular junction is made up of a nerve terminal, which contains the neurotransmitter acetylcholine, and a muscle fiber, which has receptors for acetylcholine.

When an action potential reaches the nerve terminal, it causes the release of acetylcholine, which diffuses across the synapse and binds to receptors on the muscle fiber. This activates an ion channel, allowing ions to flow into the muscle fiber and causing it to depolarize. This depolarization triggers the release of calcium ions from intracellular stores, which initiates the contraction of the muscle.

Sources

  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2018)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "End-Plate Acetylcholine Receptor: Structure, Mechanism, Pharmacology, and Disease" Physiological Reviews (2012)
  6. "Postsynaptic potentiation and desensitization at the vertebrate end-plate receptors" Progress in Neurobiology (1992)
  7. "Motor neuron, nerve, and neuromuscular junction disease" Current Opinion in Neurology (2011)