where does action potential start in a neuron
Action potential Each excitable patch of membrane has two important levels of membrane potential: the resting potential, which is the value the membrane potential maintains as long as nothing perturbs the cell, and a higher value called the threshold potential. At the axon hillock of a typical neuron, the resting potential is around –70 millivolts (mV) and the threshold potential is around –55 mV. Synaptic inputs to a neuron cause the membrane to depolarize or hyperpolarize; that is, they cause the membrane potential to rise or fall. Action potentials are triggered when enough depolarization accumulates to bring the membrane potential up to threshold. When an action potential is triggered, the membrane potential abruptly shoots upward and then equally abruptly shoots back downward, often ending below the resting level, where it remains for some period of time. The shape of the action potential is stereotyped; this means that the rise and fall usually have approximately the same amplitude and time course for all action potentials in a given cell. (Exceptions are discussed later in the article). In most neurons, the entire process takes place in about a thousandth of a second. Many types of neurons emit action potentials constantly at rates of up to 10–100 per second. However, some types are much quieter, and may go for minutes or longer without emitting any action potentials.
Pulse Pressure waves generated by the heart in systole move the arterial walls. Forward movement of blood occurs when the boundaries are pliable and compliant. These properties form enough to create a palpable pressure wave.
Cardiac action potential This phase is also known as the "plateau" phase due to the membrane potential remaining almost constant, as the membrane very, very slowly begins to repolarize. This is due to the near balance of charge moving into and out of the cell. During this phase delayed rectifier potassium channels allow potassium to leave the cell whilst L-type calcium channels (activated by the flow of sodium during phase 0), allow the movement of calcium into the cell. This calcium, binds to and opens more calcium channels (called ryanodine receptors) located on the sarcoplasmic reticulum within the cell, allowing the flow of calcium out of the SR. This calcium is responsible for contraction of the heart. Not only that, but it also activates chloride channels called Ito2, which allow Cl− to enter the cell. Together the movement of both Ca2+ and Cl− oppose the voltage change caused by K+. As well as this the increased calcium concentration increases the activity of the sodium-calcium exchanger, and the increase in sodium entering the cell increases activity of the sodium-potassium pump. The movement of all of these ions results in the membrane potential remaining relatively constant.[17][8] This phase is responsible for the large duration of the action potential and is important in preventing irregular heartbeat (cardiac arrhythmia).
Stimulus (physiology) Vision provides opportunity for the brain to perceive and respond to changes occurring around the body. Information, or stimuli, in the form of light enters the retina, where it excites a special type of neuron called a photoreceptor cell. A local graded potential begins in the photoreceptor, where it excites the cell enough for the impulse to be passed along through a track of neurons to the central nervous system. As the signal travels from photoreceptors to larger neurons, action potentials must be created for the signal to have enough strength to reach the CNS.[2] If the stimulus does not warrant a strong enough response, it is said to not reach absolute threshold, and the body does not react. However, if the stimulus is strong enough to create an action potential in neurons away from the photoreceptor, the body will integrate the information and react appropriately. Visual information is processed in the occipital lobe of the CNS, specifically in the primary visual cortex.[2]