20.7
Muscle Contraction
A voluntary skeletal muscle contraction begins in the brain as a conscious effort from the frontal lobe to the primary motor cortex, before activating, an alpha motor neuron located in the anterior horn of the spinal cord.
The signal continues down a nerve to the specific muscle fiber such as those found in the biceps, where the action potentials terminate at the motor end plate. There, the motor neuron establishes synaptic contact with the muscle fiber and triggers the release of the neuro transmitter acetylcholine, which diffuses across the synaptic cleft and binds to receptors.
As a result, the sarcolemma becomes more permeable to sodium ions, resulting in more action potentials that spread along its external surface and into the interior of the muscle fiber through transverse or T-tubules, which triggers the release of calcium ions from the sarcoplasmic reticulum into the myofibrils.
This release of calcium initiates actin-myosin crossbridge activity and the observation of the muscle shortening and contracting.
In skeletal muscles, acetylcholine is released by nerve terminals at the motor end plate—the point of synaptic communication between motor neurons and muscle fibers. Binding of acetylcholine to its receptors on the sarcolemma allows entry of sodium ions into the cell and triggers an action potential in the muscle cell. Thus, electrical signals from the brain are transmitted to the muscle. Subsequently, the enzyme acetylcholinesterase breaks down acetylcholine to prevent excessive muscle stimulation.
Individuals with the disorder myasthenia gravis, develop antibodies against the acetylcholine receptor. This prevents transmission of electrical signals between the motor neuron and muscle fiber and impairs skeletal muscle contraction. Myasthenia gravis is treated using drugs that inhibit acetylcholinesterase (allowing more opportunities for the neurotransmitter to stimulate the remaining receptors) or suppress the immune system (preventing the formation of antibodies).
Smooth Muscle Contraction
Unlike skeletal muscles, smooth muscles present in the walls of internal organs are innervated by the autonomic nervous system and undergo involuntary contractions. Contraction is mediated by the interaction between two filament proteins—actin and myosin. The interaction of actin and myosin is closely linked to intracellular calcium concentration. In response to neurotransmitter or hormone signals or stretching of the muscle, extracellular calcium enters the cell through calcium channels on the sarcolemma or is released intracellularly from the sarcoplasmic reticulum. Inside the cell, calcium binds to the regulatory protein calmodulin. The calcium-calmodulin complex then activates the enzyme myosin light chain kinase, which phosphorylates myosin and allows it to interact with actin, causing the muscle to contract.
A voluntary skeletal muscle contraction begins in the brain as a conscious effort from the frontal lobe to the primary motor cortex, before activating, an alpha motor neuron located in the anterior horn of the spinal cord.
The signal continues down a nerve to the specific muscle fiber such as those found in the biceps, where the action potentials terminate at the motor end plate. There, the motor neuron establishes synaptic contact with the muscle fiber and triggers the release of the neuro transmitter acetylcholine, which diffuses across the synaptic cleft and binds to receptors.
As a result, the sarcolemma becomes more permeable to sodium ions, resulting in more action potentials that spread along its external surface and into the interior of the muscle fiber through transverse or T-tubules, which triggers the release of calcium ions from the sarcoplasmic reticulum into the myofibrils.
This release of calcium initiates actin-myosin crossbridge activity and the observation of the muscle shortening and contracting.
From Chapter 20:
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20.7 : Muscle Contraction
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