Editing Threshold potential (section)

==Physiological function and characteristics==
{{See also|Summation (neurophysiology)}}

The threshold value controls whether or not the incoming stimuli are sufficient to generate an action potential. It relies on a balance of incoming inhibitory and excitatory stimuli. The potentials generated by the stimuli are additive, and they may reach threshold depending on their frequency and amplitude. Normal functioning of the [[central nervous system]] entails a [[Summation (neurophysiology)|summation]] of synaptic inputs made largely onto a neuron's dendritic tree. These local graded potentials, which are primarily associated with external stimuli, reach the [[axonal initial segment]] and build until they manage to reach the threshold value.{{sfn|Stuart|Spruston|Sakmann|Häusser|1997|p=127}} The larger the stimulus, the greater the [[depolarization]], or attempt to reach threshold. The task of depolarization requires several key steps that rely on anatomical factors of the cell. The ion conductances involved depend on the membrane potential and also the time after the membrane potential changes.{{sfn|Trautwein|1963|p=330}}

===Resting membrane potential===
The [[lipid bilayer|phospholipid bilayer]] of the [[cell membrane]] is, in itself, highly impermeable to ions. The complete structure of the cell membrane includes many proteins that are embedded in or completely cross the lipid bilayer. Some of those proteins allow for the highly specific passage of ions, [[ion channels]]. Leak potassium channels allow potassium to flow through the membrane in response to the disparity in concentrations of potassium inside (high concentration) and outside the cell (low). The loss of positive(+) charges of the potassium(K+) ions from the inside of the cell results in a negative potential there compared to the extracellular surface of the membrane.{{sfn|Nicholls|Martin|Fuchs|Brown|2012|p=144}} A much smaller "leak" of sodium(Na+) into the cell results in the actual resting potential, about&nbsp;–70 mV, being less negative than the calculated potential for K+ alone, the equilibrium potential, about&nbsp;–90 mV.{{sfn|Nicholls|Martin|Fuchs|Brown|2012|p=144}} The [[Na+/K+-ATPase|sodium-potassium ATPase]] is an active transporter within the membrane that pumps potassium (2 ions) back into the cell and sodium (3 ions) out of the cell, maintaining the concentrations of both ions as well as preserving the voltage polarization.

===Depolarization===
However, once a stimulus activates the voltage-gated sodium channels to open, positive sodium ions flood into the cell and the voltage increases. This process can also be initiated by ligand or neurotransmitter binding to a [[Ligand-gated ion channel|ligand-gated channel]]. More sodium is outside the cell relative to the inside, and the positive charge within the cell propels the outflow of potassium ions through delayed-rectifier voltage-gated potassium channels. Since the potassium channels within the cell membrane are delayed, any further entrance of sodium activates more and more voltage-gated sodium channels. Depolarization above threshold results in an increase in the conductance of Na sufficient for inward sodium movement to swamp outward potassium movement immediately.{{sfn|Nicholls|Martin|Fuchs|Brown|2012|p=121}} If the influx of sodium ions fails to reach threshold, then sodium conductance does not increase a sufficient amount to override the resting potassium conductance. In that case, [[subthreshold membrane potential oscillations]] are observed in some type of neurons. If successful, the sudden influx of positive charge depolarizes the membrane, and potassium is delayed in re-establishing, or hyperpolarizing, the cell. Sodium influx depolarizes the cell in attempt to establish its own equilibrium potential (about +52 mV) to make the inside of the cell more positive relative to the outside.

===Variations===
The value of threshold can vary according to numerous factors.  Changes in the ion conductances of sodium or potassium can lead to either a raised or lowered value of threshold. Additionally, the diameter of the axon, density of voltage activated sodium channels, and properties of sodium channels within the axon all affect the threshold value.{{sfn|Trautwein|1963|p=281}} Typically in the axon or dendrite, there are small depolarizing or hyperpolarizing signals resulting from a prior stimulus. The passive spread of these signals depend on the passive electrical properties of the cell. The signals can only continue along the neuron to cause an action potential further down if they are strong enough to make it past the cell's membrane resistance and capacitance. For example, a neuron with a large diameter has more ionic channels in its membrane than a smaller cell, resulting in a lower resistance to the flow of ionic current. The current spreads quicker in a cell with less resistance, and is more likely to reach the threshold at other portions of the neuron.{{sfn|Nicholls|Martin|Fuchs|Brown|2012|p=121}}

The threshold potential has also been shown experimentally to adapt to slow changes in input characteristics by regulating sodium channel density as well as inactivating these sodium channels overall. [[Hyperpolarization (biology)|Hyperpolarization]] by the delayed-rectifier potassium channels causes a [[Refractory period (physiology)#Neuronal refractory period|relative refractory period]] that makes it much more difficult to reach threshold. The delayed-rectifier potassium channels are responsible for the late outward phase of the action potential, where they open at a different voltage stimulus compared to the quickly activated sodium channels. They rectify, or repair, the balance of ions across the membrane by opening and letting potassium flow down its concentration gradient from inside to outside the cell. They close slowly as well, resulting in an outward flow of positive charge that exceeds the balance necessary. It results in excess negativity in the cell, requiring an extremely large stimulus and resulting depolarization to cause a response.