Pig Trachealis Smooth Muscle Pharmomechanical coupling uses Internal Calcium stores whilst Electromechanical coupling uses Extracellular Calcium

Contractility of ASM requires an increased levels of intracellular Ca2+. When surface receptors are not activated, Ca2+ levels are low. Upon activation of these cell surface receptors by contractile agonists e.g. acetylcholine, serotonin and histamine, intracellular Ca2+ increases causing a contraction (9). Smooth muscle cell contraction is controlled by both receptor and mechanical activation of proteins actin and myosin and also changes to membrane potential.

Voltage gated channels are necessary components of life processes, in many organisms. One in particular, is the calcium voltage gated ion channel. Often lodged within the phospholipid bilayer, the imbalance of the calcium, or, the inside vs outside concentration, creates a gradient. The channel proteins often undergo conformations, states that which allow or block calcium ions from passing through. As ions move inside the cell, this creates a depolarization, or surge in the voltage. Clinically, this is associated with the heart and how it allows the heart to contract, which can be read in the

At the cellular and tissue levels, the model can duplicate the heart's responses to changes in the levels and flow of calcium, sodium, and potassium. In addition, it can take into consideration the pace at which the ion channels - which take in those ions -

Influx and efflux of calcium regulate the membrane potential of the cell, which in turn regulates the contractility of smooth muscle cells. However, we neglected to link calcium’s role in membrane potential to its effects on potassium channels, one of the focuses of the first paper and the main influence on vasodilation and constriction. Furthermore, although external sources backed up the influence of insulin in activating Ca2+-ATPase as we wrote in our second hypothesis, the new supporting information does not mention insulin while suggesting that glucose might have a role in be inhibiting these Ca+-dependent K+

When a skeletal muscle fires it is caused by a signal in a motor neuron. Voltage gated sodium channels open up after a threshold stimulus of -55mV is reached. Next, Sodium ions move into the cell membrane, thus depolarizing the cell at +30mV, which is its action potential. Sodium channels close and Potassium channels open. Potassium moves out, which repolarizes the cell. Hyperpolarization

In order for an axon to send information, it has to release neurotransmitter stored in the synaptic vesicles in the axon terminal. In order for this to occur, Ca2+ ions must first be present in the axon terminal, and an action potential must have been initiated. This experiment will be researching if Ca2+ levels in an extracellular solution will affect the amount of neurotransmitter released at an axon terminal. Will a larger concentration of Ca2+ ions present in the extracellular fluid, induce a greater release of neurotransmitter, and if there is no Ca2+ present in the solution, will no neurotransmitter be released?

Both the actin and myosin filaments and calcium channel will cause a change in the muscle cell and move the tropomyosin towards the cross bridges and create salt bridges. The strength and duration will depend on how fast ATP

Muscles contract when the central nervous system gets a signal to contract from the brain. In order to know how muscles contract you have to know what elements create a muscle. The skeletal muscles are made up of many bundles of muscle fibers, which are long strands of multinucleate cells. The fiber is formed by the fusion of many cells. The muscle fiber’s main components are the myofibrils. The myofibrils contain sarcomeres, which is the main element responsible for the contraction and relaxation of the muscle. The contraction and relaxation actually are from the sarcomere shortening and lengthening. The sarcomere is made of thick filaments made of myosin and thin filaments composed of actin. These filaments never change in length; in fact, they slide past each other, which then allows the sarcomere to shorten the muscle to contract. In actual contraction, there is an interaction between myosin heads and the actin filament. In this interaction, a group of proteins aid in the process. Those proteins are, troponin and tropomyosin and the proteins actin and myosin that have been mentioned early that are contractile proteins (Johnson 2013).

Action potential travels across the sarcolemma and down the T-tubules which triggers the sarcoplasmic reticulum SR to release Ca+

Nerve and muscle twitch recruitment: External electrode stimulation of a nerve or muscle can lead to a twitch so long as the stimulus voltage is above the muscle or nerve’s threshold value. Electrical stimulation works to open ion channels without the muscle cells, leading to the firing of action potentials. After some time, however, a maximal stimulus voltage will be found. Voltages above this lead to no significant increase in the amplitude of the twitch. Our expectation was that twitch amplitude would increase steadily starting at threshold stimulus and level off at the maximal stimulus. These expectations were based on the results we obtained in previous labs as well as a basic understanding of action potentials, and they were met in this

The mechanism of heart contraction and relaxation (mechanical restitution) is the basic of cardiac functioning. This mechanical restitution is driven by calcium movement and concentrations. An increase in cystolic calcium concentration causes contraction in myocardium.

The contraction force of the heart is partially modulated by a small complex of proteins. Actin and myosin, the “muscles” of the muscle cell are always in close proximity, but can’t interact due to another smaller complex that interfeers with it. This complex is known as the Troponin/tropomyosin complex. The troponin component of that complex is comprised of Troponin I, Troponin T, and Troponin C. All of these proteins interact and work as an on/off switch for the heart muscle. When calcium binds to Troponin C, the Troponin.tropomyosin

2. Figure 1 for Exercise 1, shows a positive linear tread, when stimulus intensity (V) increases the contractile force (N) also increases. As the stimulus intensity increases more motor units are recruited. To emphasize, when you have a stronger stimulus the more motor unit recruitment will get excited and thus more will contract. Physiologically, a skeletal muscle membrane is getting depolarized by a stimulus. The depolarization stimulus will allow for Na+ to flow into the cell which allows the action potential to flow down into the T-tubule. The DHP receptor will open, which is connected to the RyR Ca2+ release channel to open. This allows for calcium to flow into the cytoplasm from sarcoplasmic reticulum. The calcium ion binds to troponin which allows tropomyosin to move off the actin-myosin binding sites. The myosin will bind to the actin binding site and cross bridge cycling will take place causing a muscle contraction. Therefore, the more depolarized the cells are (from a higher stimulus intensity), the more calcium will be in the cell to bind to troponin, which

2] The steps of events and cell location that leads to a release of calcium for muscle contraction, is produced by an electrical impulse which was caused by a stimulus. The impulse causes the muscle membrane to have a charge which then makes the calcium ions leave from the sarcoplasmic reticulum. When calcium and troponin are attached to each other it makes tropomyosin which move away from the actin filaments which allows the contractions to occur

Nerve conduction studies are often utilized by clinician to diagnose patients suffering neuromuscular diseases that cannot be determined by neurological examination alone. Nerve conduction velocity (NCV) measures the speed of conduction of an electrical impulse that travels through a nerve. It is an expression of the physiological state of the nerve itself. In order to determine the NCV of the Ulnar nerve, a stimulator is initially used to depolarize the nerve. A small electrical stimulus is applied to the nerve. Before the electrical stimulation, the membrane is said to be at resting potential of -70mv. If the electrical impulses is greater then the threshold potential (-55mv), then the electrical stimulus will causes the opening of the Na+ channel, permitting the influx of Na+ into the cell membrane, thus causing further depolarization of the cell membrane. The K+ channels open thereafter and leads to efflux of K+ and restoration of the resting potential of the membrane. The rapid change in the charge of the nerve is called an action potential (AP). In the Ulnar nerve, the depolarization associated with the AP travels rapidly, with little attenuation from one node of Ranvier to the next. This known as Saltatory conduction. As the AP travels down the nerve cell, it causes the release of Acetyl coenzyme A (acetyl-CoA) into the synapse. As acetyl-CoA binds to the nicotinic acetylcholine, it causes an AP in the muscle cell. AP propagates down the T tubules to the sarcoplasmic