Editing Batrachotoxin (section)

=== Neurotoxicity ===
As a [[neurotoxin]], it affects the [[nervous system]]. Neurological function depends on  [[depolarization]] of nerve and muscle fibres due to increased [[sodium]] ion permeability of the [[excitable cell membrane]]. [[Lipid-soluble]] toxins such as batrachotoxin act directly on [[sodium ion channel]]s<ref name="pmid16354762">{{cite journal |last1=Wang |first1=Sho-Ya |last2=Mitchell |first2=Jane |last3=Tikhonov |first3=Denis B. |last4=Zhorov |first4=Boris S. |last5=Wang |first5=Ging Kuo |title=How Batrachotoxin Modifies the Sodium Channel Permeation Pathway: Computer Modeling and Site-Directed Mutagenesis |journal=Molecular Pharmacology |date=March 2006 |volume=69 |issue=3 |pages=788–795 |doi=10.1124/mol.105.018200 |pmid=16354762 |s2cid=6343011 }}</ref> involved in [[action potential]] generation and by modifying both their ion selectivity and voltage sensitivity. Batrachotoxin irreversibly binds to the Na<sup>+</sup> channels which causes a conformational change in the channels that forces the sodium channels to remain open. Batrachotoxin not only keeps [[Voltage-gated ion channel|voltage-gated]] sodium channels open but also reduces single-channel conductance. In other words, the toxin binds to the sodium channel and keeps the membrane permeable to sodium ions in an "all or none" manner.<ref>{{cite journal |last1=Wang |first1=Sho-Ya |last2=Tikhonov |first2=Denis B. |last3=Mitchell |first3=Jane |last4=Zhorov |first4=Boris |last5=Wang |first5=Ging Kuo |title=Irreversible Block of Cardiac Mutant Na + Channels by Batrachotoxin |journal=Channels |date=23 May 2007 |volume=1 |issue=3 |pages=179–188 |doi=10.4161/chan.4437 |pmid=18690024 |doi-access=free }}</ref>

This has a direct effect on the [[peripheral nervous system]] (PNS). Batrachotoxin in the PNS produces increased [[Semipermeable membrane|permeability]] (selective and irreversible) of the resting cell membrane to sodium ions, without changing [[potassium]] or [[calcium]] concentration. This influx of sodium depolarizes the formerly polarized cell membrane. Batrachotoxin also alters the ion selectivity of the ion channel by increasing the permeability of the channel toward larger cations. Voltage-sensitive sodium channels become persistently active at the resting membrane potential. Batrachotoxin kills by permanently blocking nerve signal transmission to the muscles.

Batrachotoxin binds to and irreversibly opens the sodium channels of nerve cells and prevents them from closing. The neuron can no longer send signals and this results in paralysis. Furthermore, the massive influx of sodium ions produces [[osmotic]] alterations in nerves and muscles, which causes structural changes. It has been suggested that there may also be an effect on the [[central nervous system]], although it is not currently known what such an effect may be.