Acetylchoway Analysis

When a stimulus is applied to smooth muscle, it causes an action potential, depolarizing the plasma membrane. Voltage gated calcium channels open allowing calcium into the cell. This increases calcium levels in smooth muscle cells.

The voltage gated potassium-complex are made of single ion pore with subunits. Located in the postsynaptic fold. The voltage gated potassium complex has a significant amount of roles such

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.

If acetylcholine is not liberated than it would also not cause an action potential which would not cause a muscle contraction.

EDMAN KA & SCHILD HO 1962, ‘The need for calcium in the contractile response induced by acetylcholine

nerve fibers, preventing them from releasing acetylcholine, a chemical that allows nerves to communicate with muscles and other nerves.”

The ability of HVA Ca2+ channels to alter the firing pattern of postsynaptic neurons makes regulation of HVA Ca2+ channels a means to help prevent hypersynchronis neuronal activity and prevent epileptic seizures. The synaptic vesicle protein 2A (SV2A) is a protein in neurons that is important for calcium-regulated secretion of neurotransmitters (6). The protein SV2A regulates neurotransmitter release by affecting the expression of the Ca2+ sensor protein synaptotagmin, by reducing Ca2+-mediated vesicle exocytosis and thereby reducing neurotransmitter release (6). The ability of SV2A to affect synaptotagmin expression and reduce exocytosis makes regulation of SV2A binding a means to prevent abnormal neuronal activity and prevent epileptic seizures.

Information is passed between neurons and muscles through the release of neurotransmitters. These neurotransmitters are stored in synaptic vesicles in synapses. But before they can dock at a synapse, a motor transport known as kinesin moves the synaptic vesicles along microtubules to their final destination in the cell. This process is known as vesicle transport.

toxin A and E cleave a bond in SNAP-25, but A cleaves the peptide bond between Gln197-Arg198 whilst E cleaves Arg180-Ile181. Only one peptide bond in the SNARE protein is cleaved by the catalytic domain of the light chain, even though there may be more occurrences of the same bond within the structure. The reason for this was speculated to be due to structural differences between the serotypes and that the binding domain of each may be in a different position so that when the toxin binds to its substrate it changes its orientation to cleave the peptide bond that is ideal in correspondence with the change in orientation. The effect of the peptide bond cleavage is revealed once an action potential reaches the neuron. An action potential at the neuron depolarises the membrane and this causes an influx of Ca2+ ions in the axon. The formation of a neurotransmitter occurs when acetyl-CoA and choline react to produce acetylcholine in a process catalysed by the enzyme choline acetyltransferase. The calcium ions stimulate neurotransmitter release and thus acetylcholine molecules want to leave the cell via

Although both studies used the presence of markers such as horseradish peroxide to identify the membrane during the stimulation of a frog neuromuscular junction; the first of the papers by Heuser and Reese found that portions of cellular membrane at the frog neuromuscular junction were taken up by the cell and converted back into synaptic vesicles whereas ceccarelli observed no vesicle depletion but an increase in the number of labelled vesicles over time. He and his co workers propsed that vesicle fusion involves the opening of a small pore, termed ‘fusion pore’ followed by its rapid closure without full dilation and collapse at the same site of fusion. (reese, n.d.) (cecerlli, n.d.) This composes the Kiss and Run Argument but the electron microscope evidence is neither compelling or persuasive as the images are unclear where the omega membrane profile in the fixed tissue is on the way to collapsing into the plasma membrane or to closing its

Muscle contractions start when stored calcium ions are released into the cytosol. The receptor is bound to the end plate, sending an electrical signal to activate the contraction. The signal will travel to the sarcolemma in the tubule causing calcium ion to release at the point where sarcoplasmic reticulum (SR) and the T tubule meet.

When acetylcholine reaches the muscles side of neuromuscular junction, it attaches and locks into receptors. If anything interferes with these steps, the nerve will not be able to control muscle contraction. When there is an interruption of normal communication between the nerves and the muscles at the neuromuscular junction, myasthenia gravis occur. This interruption is caused by antibodies that prevent acetylcholine from reaching muscle by destroying or blocking the receptors.

Moreover, channelopathies produce changes in neurotransmitter release through alterations in calcium channels (4). Any event that disrupts

Muscle contraction begins when the nervous system generates a signal. A motor neuron conducts an action potential to the link with the muscle fiber at the neuromuscular junction a neurotransmitter called acetylcholine is released. This chemical then binds to receptors on the muscle fibers. Acetylcholine receptors are chemically gated ion channels. When Acetylcholine binds it opens and allows an influx of sodium ions into the muscle fiber. This stimulates the sarcolemma and generates another action potential that travels through tiny folds knows as transverse tubules the action potential reaches myofibrils within the muscle fiber, surrounding the myofibrils are membranous sacs called the sarcoplasmic reticulum. The arrival of the action potential

Synaptic transmission is trigger by calcium influx through voltage gated calcium channels (VGCCs). VGCCs open in response to membrane depolarization cause, in most cases, by action potentials propagating through a nerve ending. Once inside the terminal, calcium diffuses and binds to a calcium-sensing protein called synaptotagmin I, which acts as the trigger for vesicle fusion with the pre-synaptic active zone. The basic mechanisms of synaptic transmission have been extensively described in the past 70 years, but the finest details of how neurotransmitters are released in response to action potentials remain unclear. Recent work indicates that at Schaffer collateral synapses neurotransmitter release is triggered by opening of one single calcium