1) A signal from the brain travels down the spinal cord and triggers a motor neuron at the neuromuscular junction to fire.
2) This causes the release of acetylcholine into the synaptic cleft, which binds to nicotinic receptors on the muscle fiber.
3) The opening of these ligand-gated ion channels allows sodium to enter the muscle fiber, causing depolarization and triggering more sodium channels to open via a chain reaction, propagating the action potential through the muscle fiber.
1) A signal from the brain travels down the spinal cord and triggers a motor neuron at the neuromuscular junction to fire.
2) This causes the release of acetylcholine into the synaptic cleft, which binds to nicotinic receptors on the muscle fiber.
3) The opening of these ligand-gated ion channels allows sodium to enter the muscle fiber, causing depolarization and triggering more sodium channels to open via a chain reaction, propagating the action potential through the muscle fiber.
1) A signal from the brain travels down the spinal cord and triggers a motor neuron at the neuromuscular junction to fire.
2) This causes the release of acetylcholine into the synaptic cleft, which binds to nicotinic receptors on the muscle fiber.
3) The opening of these ligand-gated ion channels allows sodium to enter the muscle fiber, causing depolarization and triggering more sodium channels to open via a chain reaction, propagating the action potential through the muscle fiber.
the brain this electrochemical signal is sent from the brain down the spinal cord to the motor neuron existing at the neuromuscular Junction the motor neuron at the neuromuscular Junction will then fire an action potential the action potential is carried as positively charged sodium ions down the axon of the motor neuron when these positively charged sodium ions reach the axon terminal this triggers the opening of voltage-gated calcium channels when these channels open calcium floods into the axon terminal the presence of calcium in the axon terminal triggers the release of synaptic vesicles from their docking sites then the synaptic vesicles fuse to the presynaptic membrane and release neurotransmitter into the synaptic cleft the type of neurotransmitter used at the neuromuscular Junction is acetylcholine acetylcholine once released will passively diffuse across a synaptic cleft of the neuromuscular Junction these molecules will then bind to nicotinic acetylcholine receptors located on the muscle fiber nicotinic acetylcholine receptors are ligand gated sodium ion channels when acetylcholine binds to these receptors the ion channels open and sodium floods into the muscle fiber sodium is a positively charged ion so the ado so the addition of sodium in the muscle fiber causes a localized depolarization if there is enough depolarization nearby voltage-gated sodium channels will then open when voltage-gated sodium channels are opened there is a further influx of positively charged sodium ions entering the muscle fiber this further depolarizes the muscle fiber triggering even more voltage-gated sodium channels to open this chain reaction is the action potential this action potential is then propagated across the sarcolemma and down the t tubules when the action potential is propagated voltage-gated calcium channels located on the sarcoplasmic reticulum will open when these channels open the sarcoplasmic reticulum releases calcium ions into the sarcoplasm when calcium is in the sarcoplasm it is able to bind to troponin when calcium binds to troponin troponin will undergo a conformational change which pulls tropomyosin off of the myosin binding site now that the myosin binding site is available for binding the crossbridge cycle to begin
contraction full part 2
sliding filament theory is the mechanism
by which muscles are thought to contract at a cellular level an understanding of the structure of skeletal muscle is useful when learning how sliding filament theory works each muscle is made up of a number of bundles of muscle fibers each bundle of muscle fibers contains anywhere from ten and a hundred individual fibers each muscle fiber itself contains cylindrical organelles known as myofibrils which themselves are bundles of proteins called actin and myosin surrounding the myofibril there is a network of tubules and channels called the sarcoplasmic reticulum where calcium is stored each myofibril can be broken down into functional repeating segments called sarcomeres if we look at a two-dimensional model of a sarcomere it consists of actin and myosin when a nerve impulse arrives at the muscle it causes a release of a chemical called acetylcholine the presence of acetylcholine causes depolarization enabling calcium to be released from the sarcoplasmic reticulum the calcium binds to troponin changing its shape and so moving tropomyosin from the active site of the actin the myosin filaments can now attach to the actin forming a cross bridge the breakdown of ATP releases energy which enables the myosin to pull the actin filaments inwards contracting the muscle this occurs along the entire length of every myofibril in the muscle cell when an ATP molecule binds to the myosin head the myosin detaches from the actin and the cross bridge is broken when the ATP is then broken down the myosin head can again attach to an actin binding site further along the actin filament and repeat the process this repeated pulling of the actin over the myosin is often known as the ratchet mechanism this process of muscular contraction can last for as long as there are adequate ATP and ca+ stores once the nerve impulse stops the ca+ is pumped back to the sarcoplasmic reticulum and the actin returns to its resting position causing the muscle to lengthen and relax you