Editing Action potential (section)

=== Maturation of the electrical properties of the action potential ===
A [[neuron]]'s ability to generate and propagate an action potential changes during [[Neural development|development]]. How much the [[membrane potential]] of a neuron changes as the result of a current impulse is a function of the membrane [[Input impedance|input resistance]]. As a cell grows, more [[Ion channel|channels]] are added to the membrane, causing a decrease in input resistance. A mature neuron also undergoes shorter changes in membrane potential in response to synaptic currents. Neurons from a ferret [[lateral geniculate nucleus]] have a longer [[time constant]] and larger [[voltage]] deflection at P0 than they do at P30.<ref name=":0">{{Cite book|title=Development of the nervous system|last1=Sanes|first1=Dan H.|last2=Reh|first2=Thomas A | name-list-style = vanc |date=2012-01-01|publisher=Elsevier Academic Press|isbn=9780080923208|pages=211–214|oclc=762720374|edition=Third}}</ref> One consequence of the decreasing action potential duration is that the fidelity of the signal can be preserved in response to high frequency stimulation. Immature neurons are more prone to synaptic depression than potentiation after high frequency stimulation.<ref name=":0" />

In the early development of many organisms, the action potential is actually initially carried by [[Calcium channel|calcium current]] rather than [[Sodium channel|sodium current]]. The [[Gating (electrophysiology)|opening and closing kinetics]] of calcium channels during development are slower than those of the voltage-gated sodium channels that will carry the action potential in the mature neurons. The longer opening times for the calcium channels can lead to action potentials that are considerably slower than those of mature neurons.<ref name=":0" /> [[Xenopus]] neurons initially have action potentials that take 60–90 ms. During development, this time decreases to 1 ms. There are two reasons for this drastic decrease. First, the [[Depolarization|inward current]] becomes primarily carried by sodium channels.<ref>{{Cite book|title=Calcium Channels: Their Properties, Functions, Regulation, and Clinical relevance|last=Partridge|first=Donald | name-list-style = vanc |publisher=CRC Press|year=1991|isbn=9780849388071|pages=138–142}}</ref> Second, the [[Voltage-gated potassium channel|delayed rectifier]], a [[potassium channel]] current, increases to 3.5 times its initial strength.<ref name=":0" />

In order for the transition from a calcium-dependent action potential to a sodium-dependent action potential to proceed new channels must be added to the membrane. If Xenopus neurons are grown in an environment with [[Transcription (biology)|RNA synthesis]] or [[Translation (biology)|protein synthesis]] inhibitors that transition is prevented.<ref>{{Cite book|url=https://www.springer.com/us/book/9780306415500|title=Cellular and Molecular Biology of Neuronal Development {{!}} Ira Black {{!}} Springer|last=Black|first=Ira | name-list-style = vanc |publisher=Springer|year=1984|isbn=978-1-4613-2717-2|pages=103|language=en|url-status=live|archive-url=https://web.archive.org/web/20170717154858/http://www.springer.com/us/book/9780306415500|archive-date=17 July 2017|df=dmy-all}}</ref> Even the electrical activity of the cell itself may play a role in channel expression. If action potentials in Xenopus [[myocyte]]s are blocked, the typical increase in sodium and potassium current density is prevented or delayed.<ref>{{Cite book|title=Current Topics in Developmental Biology, Volume 39|last=Pedersen|first=Roger | name-list-style = vanc |publisher=Elsevier Academic Press|year=1998|isbn=9780080584621|url=https://archive.org/details/currenttopicsind0000unse_x6e1}}</ref>

This maturation of electrical properties is seen across species. Xenopus sodium and potassium currents increase drastically after a neuron goes through its final phase of [[mitosis]]. The sodium current density of rat [[Cerebral cortex|cortical neurons]] increases by 600% within the first two postnatal weeks.<ref name=":0" />