End-plate potential

End plate potentials (EPPs) are the voltages which cause depolarization of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction. They are called 'end plates' because the postsynaptic terminals of muscle fibers have a large, saucer-like appearance. When an action potential reaches the axon terminal of a motor neuron, vesicles carrying neurotransmitters (mostly acetylcholine) are exocytosed and the contents are released into the neuromuscular junction. These neurotransmitters bind to receptors on the postsynaptic membrane and lead to its depolarization. In the absence of an action potential, acetylcholine vesicles spontaneously leak into the neuromuscular junction and cause very small depolarizations in the postsynaptic membrane. This small response (~0.4mV) is called a miniature end plate potential (MEPP) and is generated by one acetylcholine-containing vesicle. It represents the smallest possible depolarization which can be induced in a muscle. End plate potentials (EPPs) are the voltages which cause depolarization of skeletal muscle fibers caused by neurotransmitters binding to the postsynaptic membrane in the neuromuscular junction. They are called 'end plates' because the postsynaptic terminals of muscle fibers have a large, saucer-like appearance. When an action potential reaches the axon terminal of a motor neuron, vesicles carrying neurotransmitters (mostly acetylcholine) are exocytosed and the contents are released into the neuromuscular junction. These neurotransmitters bind to receptors on the postsynaptic membrane and lead to its depolarization. In the absence of an action potential, acetylcholine vesicles spontaneously leak into the neuromuscular junction and cause very small depolarizations in the postsynaptic membrane. This small response (~0.4mV) is called a miniature end plate potential (MEPP) and is generated by one acetylcholine-containing vesicle. It represents the smallest possible depolarization which can be induced in a muscle. The neuromuscular junction is the synapse that is formed between an alpha motor neuron (α-MN) and the skeletal muscle fiber. When a muscle contracts, an action potential is propagated down a nerve until it reaches the axon terminal of the motor neuron. The motor neuron then innervates the muscle fibers to contraction by causing an action potential on the postsynaptic membrane of the neuromuscular junction. End plate potentials are produced almost entirely by the neurotransmitter acetylcholine in skeletal muscle. Acetylcholine is the second most important excitatory neurotransmitter in the body following glutamate. It controls the somatosensory system which includes the senses of touch, vision, and hearing. It was the first neurotransmitter to be identified in 1914 by Henry Dale. Acetylcholine is synthesized in the cytoplasm of the neuron from choline and acetyl-CoA. Choline acyltransferase is the enzyme that synthesizes acetylcholine and is often used as a marker in research relating to acetylcholine production. Neurons that utilize acetylcholine are called cholinergic neurons and they are very important in muscle contraction, memory, and learning. The polarization of membranes is controlled by sodium, potassium, calcium, and chloride ion channels. There are two types of ion channels involved in the neuromuscular junction and end plate potentials: voltage-gated ion channel and ligand-gated ion channel. Voltage gated ion channels are responsive to changes in membrane voltage which cause the voltage gated ion channel to open and allows certain ions to pass through. Ligand gated ion channels are responsive to certain molecules such as neurotransmitters. The binding of a ligand to the receptor on the ion channel protein causes a conformational change which allows the passing of certain ions. Normally the resting membrane potential of a motor neuron is kept at -70mV to -50 with a higher concentration of sodium outside and a higher concentration of potassium inside. When an action potential propagates down a nerve and reaches the axon terminal of the motor neuron, the change in membrane voltage causes the calcium voltage gated ion channels to open allowing for an influx of calcium ions. These calcium ions cause the acetylcholine vesicles attached to the presynaptic membrane to release acetylcholine via exocytosis into the synaptic cleft. EPP are caused mostly by the binding of acetylcholine to receptors in the postsynaptic membrane. There are two different kinds of acetylcholine receptors: nicotinic and muscarinic. Nicotinic receptors are ligand gated ion channels for fast transmission. All acetylcholine receptors in the neuromuscular junction are nicotinic. Muscarinic receptors are G protein-coupled receptors that use a second messenger. These receptors are slow and therefore are unable to measure a miniature end plate potential (MEPP). They are located in the parasympathetic nervous system such as in the vagus nerve and the gastrointestinal tract. During fetal development acetylcholine receptors are concentrated on the postsynaptic membrane and the entire surface of the nerve terminal in the growing embryo is covered even before a signal is fired. Five subunits consisting of four different proteins from four different genes comprise the nicotinic acetylcholine receptors therefore their packaging and assembly is a very complicated process with many different factors. The enzyme muscle-specific kinase (MuSK) initiates signaling processes in the developing postsynaptic muscle cell. It stabilizes the postsynaptic acetylcholine receptor clusters, facilitates the transcription of synaptic genes by muscle fiber nuclei, and triggers differentiation of the axon growth cone to form a differentiated nerve terminal. Substrate laminin induces advanced maturation of the acetylcholine receptor clusters on the surfaces of myotubes. All neurotransmitters are released into the synaptic cleft via exocytosis from synaptic vesicles. Two kinds of neurotransmitter vesicles exist: large dense core vesicles and small clear core vesicles. Large dense core vesicles contain neuropeptides and large neurotransmitters that are created in the cell body of the neuron and then transported via fast axonal transport down to the axon terminal. Small clear core vesicles transport small molecule neurotransmitters that are synthesized locally in the presynaptic terminals. Finalized neurotransmitter vesicles are bound to the presynaptic membrane. When an action potential propagates down the motor neuron axon and arrives at the axon terminal, it causes a depolarization of the axon terminal and opens calcium channels. This causes the release of the neurotransmitters via vesicle exocytosis.