...repolarization
Triggering of the muscle action potential occurs after acetylcholine binds to chemically-gated channels in the end plate membrane.
A potassium enhanced intravenous solution would increase the concentration of potassium ions in the brain. Since potassium ions are positively charged, they depolarize the resting membrane potential. For example, a resting membrane potential of -65 millivolts would be depolarized to -62 millivolts. An appropriate concentration could lead to a significant depolarization of, say, -60 millivolts, at which point an action potential could be possible.
The generation of a second action in some neurons can only happen after a refractory period, when the membrane potential has returned it's base level or even more negative. This is because some types of Na+ channels inactivate at a positive potential and then require a negative potential to reset. Other neurons have other types of channels and can fire multiple action potentials to a single depolarization.
An excitatory postsynaptic potential, a type of graded potential, occurs because of the influx of Na+ through chemically gated channels in the receptive region, or postsynaptic membrane, of a neuron. Graded potentials are generated by chemically gated channels, whereas action potentials are produced by voltage-gated channels.
axonsAction Potential and Axon Conduction- Resting membrane potential provides and immediate source of power (it can cause a rapid change)- Hyperpolarize - makes membrane potential more negative- Depolarize - makes membrane potential less negativeo Depolarization reaches a threshold, at this threshold you cause a massive electrical change (Action Potential aka Impulse aka Spike)- Threshold - generally 15mV above resting membrane potentialo Threshold for a neuron is around -70 less 15 = -55mV- All-or-none lawo Size of action potential for a given neuron is always the same regardless of the size of the stimulus that initiated it- Information about Magnitudeo Conveyed by frequency of action potentials (#/sec [Hz])- Alternative to Action Potential:o Graded Potential - passive change occurso Signal gets smaller and smaller as it moves on - such as some neurons found in the eyesMolecular Basis of Action Potential- Depolarizationo Results in sodium membrane "channels" or "gates" begin to open- At threshold, the number of open channels overcomes the sodium-potassium pumpo The channels have a time-limit and once open will automatically close after ½ msec.- Sodium current makes membrane potential positive, and at peak, sodium channels close and potassium channels open- Now, potassium channels open and potassium ions rush out (triggered by threshold, but have a delay to open so open after the sodium channels)- Brief hyperpolarization (voltage surpasses -70mV) while sodium potassium pump restores ion distribution- These voltage-dependant (activated) channels define the action potential- Sustained activity leads to an increase in extra-cellular potassium (typically picked up by astrocytes)- Glial cell (astrocytes) transports excess potassium to nearby arteries causing a dilation of the artery wallo More active areas need more oxygen and glucose, so the movement of the potassium to the arteries, cause them to dilate and thus allow more volume of blood (and nutrients) to the area- Refractory period - period when the cell is resistant to the generation of further action potentialso Restricts the firing rate of the cell- Two phases of the refractory period:o Absolute - no firing regardless of the size of the stimuluso Relative - threshold is higher than normalConduction of the Nerve Impulse- Action potential is regenerated at each adjacent patch of the membrane (because of diffusing sodium from generation of action potential)- Cannot move backwards - seen as a wave rather than distinct action potentials because the patches are so small, and it moves so fast- Called the propagation of the action potential- Slower than conduction of electricity down a copper wire (1-10m/sec vs. 300million m/sec)- Axons with myelin sheaths are faster (120m/sec)o Myelin sheath insulates the axon, so that sodium ions cannot pass into or out of the cello Sodium can cross at Nodes of Ranvier to generate a new action potentialo From one Node to the next, a graded potential regenerates a new action potential at the next nodeo Called "salutatory conduction"
voltage-gated potassium channels taking some time to close in response to the negative membrane potential
The action potential has 5 main phases:1) stimulation/rising phase - depolarization caused by influx of sodium ions at the axon hillock; potential increases from a resting potential of -70 mV2) peak phase - depolarization and membrane potential reaches a peak, with sodium channels open maximally, at about +40 mV3) falling phase - potassium channels open in response, causing a subsequent reduction in membrane potential, and the neuron begins to repolarize4) hyperpolarization/undershoot phase - more potassium channels stay open after sodium channels close, causing a hyperpolarization of the neuronal membrane, bringing the potential down below its initial resting potential (below -70 mV)5) refractory phase - potassium channels begin to close, allowing the membrane potential to revert back to the resting potential of -70 mV; during this phase, the probability of the nerve being able to refire is extremely low, thus allowing for a delay between action potentials
As the action potential passes an area on the axon, sodium channels are closed, preventing influx of more sodium ions. At the same time, voltage-sensitive potassium channels open, allowing the membrane potential to fall quickly. After this repolarization phase, membrane permeability to potassium remains high, allowing for the "afterhyperpolarization" phase. During this entire period, while the sodium ion channels are forced closed, another action potential cannot be generated except by a much larger input signal. This helps to prevent the action potential from moving backwards along the axon.
As the action potential passes an area on the axon, sodium channels are closed, preventing influx of more sodium ions. At the same time, voltage-sensitive potassium channels open, allowing the membrane potential to fall quickly. After this repolarization phase, membrane permeability to potassium remains high, allowing for the "afterhyperpolarization" phase. During this entire period, while the sodium ion channels are forced closed, another action potential cannot be generated except by a much larger input signal. This helps to prevent the action potential from moving backwards along the axon.
When a nerve impulse is conducted, the neuronal cell membrane undergoes changes in electrical potential. This starts with a rapid influx of sodium ions into the cell through voltage-gated sodium channels, depolarizing the membrane. This depolarization triggers the opening of adjacent sodium channels, resulting in an action potential that travels along the membrane. After the impulse passes, the sodium channels close, and potassium channels open, allowing potassium ions to exit the cell and restore the resting potential.
Sodium and potassium voltage gated ion channels.
during action potentials, sodium and potassium cross the membrane of the synapse after the threshold of membrane potential is reached. There, sodium leaves the synapse and the membrane potential is now positive. this is known as depolarization. then during repolarization, the sodium channels close and the potassium channels open to stabilize the membrane potential. during this time, a second action potential cannot occur and this is an evolutionary advantage because it allows rest in the nerve cells and it allows the membrane potential to equalize.
voltage-sensitive potassium channels
The hyperpolarization of the membrane potential relative to the resting potential (the undershoot) causes voltage-dependent Potassium conductance (and any Sodium channels not yet inactivated) to turn off, allowing the membrane potential to return to resting level.
During resting potential, the Sodium-Potassium pump is inactive. Therefore, it is indirectly responsible for the resting potential. However, Potassium diffuses outside the membrane via "leakage" channels, and causes the resting potential.
An action potential starts when sodium channels in a neuron end open and sodium ions rush is, depolarizing the neuron's membrane.
During an action potential, the neuron undergoes a rapid change in membrane potential as sodium ions rush into the cell, leading to depolarization. Subsequently, potassium ions move out of the cell, repolarizing the membrane back to its resting state. This rapid change in membrane potential allows for the transmission of electrical signals along the neuron.