Muscle Formation Case Study Essay

2. Novocain blocks action potential production at the site of injection. How do you think Novocain works on the axon membrane, and how does it block the sensation of pain?

AChE is found in red blood cells, cholinergic fibres and muscle (motor end-plate), existing as mainly membrane bound (Rang & Dale, 2007). It is highly specific for the neurotransmitter acetylcholine (ACh) and its principle role is termination of impulse

Muscle contraction can be understood as the consequence of a process of transmission of action potentials from one neuron to another. A chemical called acetylcholine is the neurotransmitter released from the presynaptic neuron. As the postsynaptic cells on the muscle cell membrane receive the acetylcholine, the channels for the cations sodium and potassium are opened. These cations produce a net depolarization of the cell membrane and this electrical signal travels along the muscle fibers. Through the movement of calcium ions, the muscle action potential is taken into actual muscle contraction with the interaction of two types of proteins, actin and myosin.

The muscarinic AChRs occur primarily in the CNS, and are part of a large family of G-protein-coupled receptors (‘G proteins’), which use an intracellular secondary messenger system involving an increase of intracellular calcium to transmit signals inside cells. Binding of acetylcholine to a muscarinic AChR causes a conformational change in the receptor that is responsible for its association with and activation of an intracellular G protein, the latter converting GTP to GDP in order to become activated and dissociate from the receptor. The activated G

Südhof discovered in his 1990 paper Phospholipid binding by a synaptic vesicle protein homologous to the regulatory region of protein kinase C that vesicle binding is a specific and precise process that is regulated by neurotransmitter release. The release of vesicles for membrane bidding is monitored by the influxes of Ca2+ ions into the cell. An increase of Ca2+ triggers the vesicle to bind to the phospholipid bilayer of a cell. Once bound the Ca2+ triggers a neurotransmitter that signals the bound vesicle to release its contents into the cell membrane by exocytosis. Südhof also confirmed that in order for certain vesicle to bind to target membranes a SNARE protein complex must be present in order to promote vesicle binding.

B) Hormonal signaling is important between cells that are at greater distances apart than in synaptic signaling.

Although there are some differences in putative mechanisms, all of the CIs are believed to function in the same basic manner - to increase the bioavailability of acetylcholine at the synapse. The acetylcholine molecule is released into the synaptic space by the presynaptic neuron and binds to receptors in the postsynaptic neuron, promoting an action potential. The acetylcholine molecule is subject to enzymatic degradation in the synaptic space by one of several cholinesterases. CIs bind to and inactivate these cholinesterases, reducing the normal enzymatic degradation of the acetylcholine molecule into its component parts (acetyl CoA and choline).

Regulates neurotransmitter discharge by slowing the recycling of the fusion machinery and down-regulating synaptic vesicle turnover (Horowitz, Lugassy, Rapaport, and Sprecher 2010)

Diazinon is a synthetic OP acaricide and insecticide widely used for veterinary and agricul-tural purposes; its animal and human exposure leads to nephrotoxicity (Pizzurro et al., 2014). Normally, chemical impulses are transmitted from the end of one nerve cell to the beginning of another in a synaptic cleft; one of the chemical transmitters used in animal nervous systems is called acetylcholine (ACh). After transmitting the nerve impulse, acetylcholine is destroyed by an enzyme called acetylcholinesterase (AChE); this helping to clear the way for another trans-mission. Organophosphates attach to AChE and prevent it from destroying acetylcholine, causing overstimulation of the nerves (Ware, 2000). Abdel-Daim (2014) confirmed that, DZN functions as an acetylcholinesterase (AChE) inhibitor. This enzyme breaks down the neurotransmitter acetylcholine (ACh) into choline and an acetate group. The inhibition of the AChE causes an ab-normal accumulation of ACh in the synaptic cleft.

As soon as the electrical signal reaches the end of the axon, mechanism of chemical alteration initiates. First, calcium ion spurt into the axon terminal, leading to the release of neurotransmitters “molecules released neurons which carries information to the adjacent cell”. Next, inside the axon terminal, neurotransmitter molecules are stored inside a membrane sac called vesicle. Finally, the neurotransmitter molecule is then discharged in synapse space to be delivered to post synaptic neuron.

Cross-bridge cycling forms the basis for movement and force production in muscle cells. Each cycle of myosin binding to actin and movement of the thin filament involves the hydrolysis of one ATP molecule. The cross- bridge is the globular head of a myosin molecule that projects from a myosin filament in muscle and in the sliding filament hypothesis of muscle contraction is held to attach temporarily to an adjacent actin filament and draw it into the A band of a sarcomere between the myosin

Step 4: Acetylcholinesterase (AChE) breaks down all of the ACh in the synaptic cleft and removes it from the postsynaptic ending. The AChE does this by hydrolyzing the ACh molecules into acetate and choline. The presynaptic knob then absorbs the choline from the synaptic cleft. The choline molecules are used to remake ACh. When ACh molecules are recycled, the recycling and transport mechanisms may not be able to keep up with the neurotransmitter. This results in synaptic fatigue, where the synapse is inactive until ACh is replenished.

1. Introductions
 Muscle tissues are one of the essential materials in human body, it plays a great role of human body, supporting not only external movement but also internal function, providing the force to help the organ 's function, for example, cardiac muscle tissue pumps the blood through the heart, making the circulatory system works fluently in human body. "Like the other collagen-based tissues which can evolve different hierarchical structures to meet their different mechanical needs"[1], the development of muscle tissues is analogous to this evolvement of mechanism, it can apparently change their quantity and quality through frequently physical activities and food intake, providing a corresponding strength to meet the "environmental change". To respond the "environmental changes," muscle tissue would be reconstructed by itself.

The main cellular process, as mentioned above, for which the Na/K-ATPase is responsible, is the maintenance of a membrane potential via the movements of its bonding ions. It is the maintenance, and the presence of this potential that allow the existence of the cell. The presence of a pre-existing potential allows transport of glucose and other molecules, such as Cl- ions via the mechanism of secondary active transport, harnessing the Na+ gradient into the cell caused by ATP breakdown (Skou 2004).

One thing that is important to keep in mind about these circuits are the release of neurotransmitters. The image 1 summarizes it. Note the secretion of dopamine, an inhibitory neurotransmitter in most parts of the brain, from the substantia nigra to the caudate nucleus and putamen. It’s also important to mention that GABA (gamma-aminobutyric acid) is a inhibitory neurotransmitter that provides loops of negative feedback within the central nervous system.