View source for Neurotoxin

{{short description|Toxin harmful to nervous tissue}}
{{redirect|Neurotoxicology|the scientific journal|Neurotoxicology (journal)}}
{{distinguish|nerve agent}}
[[File:Cyanobacterial Scum.JPG|thumb|300px|right|Neurotoxins can be found in a number of organisms, including some strains of [[cyanobacteria]],<ref>{{cite journal | last1 = Sivonen | first1 = K | year = 1999 | title = Toxins produced by cyanobacteria | journal = Vesitalous | volume = 5 | pages = 11–18 }}</ref> that can be found in [[algal bloom]]s or washed up on [[shore]] in a green scum.<ref>Scottish Government [http://www.scotland.gov.uk/Publications/2002/05/14852/5357 Blue-Green Algae (Cyanobacteria) in Inland Waters: Assessment and Control of Risks to Public Health] Retrieved 15 December 2011.</ref>]]

'''Neurotoxins''' are [[toxin]]s that are destructive to [[nervous tissue|nerve tissue]] (causing [[neurotoxicity]]).<ref>Dorland's Medical Dictionary for Health Consumers</ref> Neurotoxins are an extensive class of [[exogenous]] chemical [[neurological]] [[insult (medical)|insults]]<ref name=Spencer2000>Spencer 2000</ref> that can adversely affect function in both developing and mature nervous tissue.<ref name=Olney2002>Olney 2002</ref> The term can also be used to classify [[endogenous]] compounds, which, when abnormally contacted, can prove neurologically toxic.<ref name=Spencer2000 /> Though neurotoxins are often neurologically destructive, their ability to specifically target neural components is important in the study of nervous systems.<ref name=Kiernan2005 /> Common examples of neurotoxins include [[lead]],<ref>Lidsky 2003</ref> [[ethanol]] (drinking alcohol),<ref name=Heaton2000>{{cite journal | last1 = Heaton | last2 = Barrow | first2 = Marieta | last3 = Mitchell | first3 = J. Jean | last4 = Paiva | first4 = Michael | year = 2000 | title = Amelioration of Ethanol-Induced Neurotoxicity in the Neonatal Rat Central Nervous System by Antioxidant Therapy | journal = Alcoholism: Clinical and Experimental Research | volume = 24 | issue = 4| pages = 512–18 | doi=10.1111/j.1530-0277.2000.tb02019.x| pmid = 10798588 }}</ref> [[glutamate]],<ref name=Choi1987>Choi 1987</ref> [[nitric oxide]],<ref>Zhang 1994</ref> [[botulinum toxin]] (e.g. Botox),<ref name=Rosales1996>{{cite journal | last1 = Rosales | first1 = Raymond L. | last2 = Arimura | first2 = Kimiyoshi | last3 = Takenaga | first3 = Satoshi | last4 = Osame | first4 = Mitsuhiro | year = 1996 | title = Extrafusal and Intrafusal Muscle Effects in Experimental Botulinum Toxin-A Injection | journal = Muscle & Nerve | volume = 19 | issue = 4| pages = 488–96 | doi=10.1002/(sici)1097-4598(199604)19:4<488::aid-mus9>3.0.co;2-8| pmid = 8622728 | s2cid = 20849034 }}</ref> [[tetanus toxin]],<ref name=Simpson1986>Simpson 1986</ref> and [[tetrodotoxin]].<ref name=Kiernan2005 /> Some substances such as [[nitric oxide]] and [[glutamate]] are in fact essential for proper function of the body and only exert neurotoxic effects at excessive concentrations.

Neurotoxins inhibit [[neuron]] control over [[ion]] concentrations across the [[Cell (biology)|cell]] membrane,<ref name=Kiernan2005 /> or communication between neurons across a [[synapse]].<ref name=Arnon2001>Arnon 2001</ref> Local [[pathology]] of neurotoxin exposure often includes neuron [[excitotoxicity]] or [[apoptosis]]<ref name=Dikranian2001>Dikranian 2001</ref> but can also include [[glial cell]] damage.<ref name=Deng2003>Deng 2003</ref> Macroscopic manifestations of neurotoxin exposure can include widespread [[central nervous system]] damage such as [[intellectual disability]],<ref name=Olney2002 /> persistent [[memory]] impairments,<ref>Jevtovic-Todorovic 2003</ref> [[epilepsy]], and [[dementia]].<ref>Nadler 1978</ref> Additionally, neurotoxin-mediated [[peripheral nervous system]] damage such as [[neuropathy]] or [[myopathy]] is common. Support has been shown for a number of treatments aimed at attenuating neurotoxin-mediated injury, such as [[antioxidant]]<ref name=Heaton2000 /> and [[antitoxin]]<ref name=Thyagarajan2009>Thyagarajan 2009</ref> administration.

==Background==
[[File:Complete neuron cell diagram en.svg|thumb|upright=1.5|alt=Complete labeled neuron.|Illustration of typical multipolar neuron]]

Exposure to neurotoxins in society is not new,<ref>[https://file.io/JFxJRagTfGOe Neurotoxins: Definition, Epidemiology, Etiology]</ref> as civilizations have been exposed to neurologically destructive compounds for thousands of years. One notable example is the possible significant lead exposure during the [[Roman Empire]] resulting from the development of extensive [[plumbing|plumbing networks]] and the habit of boiling vinegared wine in lead pans to sweeten it. The process generates [[lead acetate]], known as "sugar of lead".<ref>Hodge 2002</ref> In part, neurotoxins have been part of [[human]] history because of the fragile and susceptible nature of the nervous system, making it highly prone to disruption.

The nervous tissue found in the [[brain]], [[spinal cord]], and periphery comprises an extraordinarily complex biological system that largely defines many of the unique traits of individuals. As with any highly complex system, however, even small perturbations to its environment can lead to significant functional disruptions. Properties leading to the susceptibility of nervous tissue include a high surface area of neurons, a high [[lipid]] content which retains lipophilic toxins, high [[blood]] flow to the brain inducing increased effective toxin exposure, and the persistence of neurons through an individual's lifetime, leading to compounding of damages.<ref name=Dobbs2009>Dobbs 2009</ref> As a result, the nervous system has a number of mechanisms designed to protect it from internal and external assaults, including the blood brain barrier.

The [[blood–brain barrier]] (BBB) is one critical example of protection which prevents toxins and other adverse compounds from reaching the brain.<ref name=Widmaier2008>Widmaier, Eric P., Hershel Raff, Kevin T. Strang, and Arthur J. Vander (2008) Vander's Human Physiology: the Mechanisms of Body Function.' Boston: McGraw-Hill Higher Education.</ref> As the brain requires nutrient entry and waste removal, it is perfused by blood flow. Blood can carry a number of ingested toxins, however, which would induce significant neuron death if they reach nervous tissue. Thus, protective cells termed [[astrocyte]]s surround the capillaries in the brain and absorb nutrients from the blood and subsequently transport them to the neurons, effectively isolating the brain from a number of potential chemical insults.<ref name=Widmaier2008 />

[[File:Blood Brain Barriere.jpg|thumb|left|upright=1.5|alt=Blood Brain Barrier.|Astrocytes surrounding capillaries in the brain to form the blood brain barrier]]

This barrier creates a tight [[hydrophobic]] layer around the [[capillary|capillaries]] in the brain, inhibiting the transport of large or [[hydrophilic]] compounds. In addition to the BBB, the [[choroid plexus]] provides a layer of protection against toxin absorption in the brain. The choroid plexuses are vascularized layers of tissue found in the third, fourth, and lateral [[ventricular system|ventricles of the brain]], which through the function of their [[ependymal]] cells, are responsible for the synthesis of [[cerebrospinal fluid]] (CSF).<ref name=Martini2009>Martini 2009</ref> Importantly, through selective passage of [[ions]] and nutrients and trapping [[heavy metals]] such as lead, the choroid plexuses maintain a strictly regulated environment which contains the brain and spinal cord.<ref name=Widmaier2008 /><ref name=Martini2009 />

[[File:Gray749.png|thumb|alt=Choroid plexus.|{{center|Choroid plexus}}]]

By being hydrophobic and small, or inhibiting astrocyte function, some compounds including certain neurotoxins are able to penetrate into the brain and induce significant damage. In modern times, [[scientist]]s and [[physician]]s have been presented with the challenge of identifying and treating neurotoxins, which has resulted in a growing interest in both neurotoxicology research and clinical studies.<ref name=Costa2011>Costa 2011</ref> Though clinical neurotoxicology is largely a burgeoning field, extensive inroads have been made in the identification of many environmental neurotoxins leading to the classification of 750 to 1000 known potentially neurotoxic compounds.<ref name=Dobbs2009 /> Due to the critical importance of finding neurotoxins in common environments, specific protocols have been developed by the [[United States Environmental Protection Agency]] (EPA) for testing and determining neurotoxic effects of compounds (USEPA 1998). Additionally, [[in vitro]] systems have increased in use as they provide significant improvements over the more common [[in vivo]] systems of the past. Examples of improvements include tractable, uniform environments, and the elimination of contaminating effects of systemic metabolism.<ref name=Costa2011 /> In vitro systems, however, have presented problems as it has been difficult to properly replicate the complexities of the nervous system, such as the interactions between supporting astrocytes and neurons in creating the BBB.<ref>Harry 1998</ref> To even further complicate the process of determining neurotoxins when testing in-vitro, [[neurotoxicity]] and cytotoxicity may be difficult to distinguish as exposing neurons directly to compounds may not be possible in-vivo, as it is in-vitro. Additionally, the response of [[cell (biology)|cells]] to chemicals may not accurately convey a distinction between neurotoxins and cytotoxins, as symptoms like [[oxidative stress]] or [[human skeleton|skeletal]] modifications may occur in response to either.<ref>Gartlon 2006</ref>

In an effort to address this complication, [[neurite]] outgrowths (either axonal or dendritic) in response to applied compounds have recently been proposed as a more accurate distinction between true neurotoxins and [[cytotoxin]]s in an in-vitro testing environment. Due to the significant inaccuracies associated with this process, however, it has been slow in gaining widespread support.<ref>{{cite journal | last1 = Radio | first1 = Nicholas M. | last2 = Mundy | first2 = William R. | year = 2008 | title = Developmental Neurotoxicity Testing in Vitro: Models for Assessing Chemical Effects on Neurite Out-growth | url = https://zenodo.org/record/1259251| journal = NeuroToxicology | volume = 29 | issue = 3| pages = 361–376| doi=10.1016/j.neuro.2008.02.011| pmid = 18403021 | bibcode = 2008NeuTx..29..361R }}</ref> Additionally, biochemical mechanisms have become more widely used in neurotoxin testing, such that compounds can be screened for sufficiency to induce cell mechanism interference, like the inhibition of [[acetylcholinesterase]] capacity of [[organophosphate]]s (includes [[parathion]] and [[sarin]] gas).<ref>Lotti 2005</ref> Though methods of determining neurotoxicity still require significant development, the identification of deleterious compounds and toxin exposure symptoms has undergone significant improvement.

==Applications in neuroscience==
Though diverse in chemical properties and functions, neurotoxins share the common property that they act by some mechanism leading to either the disruption or destruction of necessary components within the [[nervous system]]. Neurotoxins, however, by their very design can be very useful in the field of [[neuroscience]]. As the nervous system in most organisms is both highly complex and necessary for survival, it has naturally become a target for attack by both predators and prey. As [[venom|venomous organisms]] often use their neurotoxins to subdue a predator or prey very rapidly, toxins have evolved to become highly specific to their target channels such that the toxin does not readily bind other targets<ref name=Adams2003>Adams 2003</ref> (see [[:Category:Ion channel toxins|Ion Channel toxins]]). As such, neurotoxins provide an effective means by which certain elements of the nervous system may be accurately and efficiently targeted. An early example of neurotoxin based targeting used [[isotopic labeling|radiolabeled]] tetrodotoxin to assay [[sodium channel]]s and obtain precise measurements about their concentration along nerve [[cell membrane|membranes]].<ref name=Adams2003 /> Likewise through isolation of certain channel activities, neurotoxins have provided the ability to improve the original [[Hodgkin–Huxley model|Hodgkin-Huxley model]] of the neuron in which it was theorized that single generic sodium and [[potassium channel]]s could account for most nervous tissue function.<ref name=Adams2003 /> From this basic understanding, the use of common compounds such as tetrodotoxin, [[tetraethylammonium]], and [[bungarotoxin]]s have led to a much deeper understanding of the distinct ways in which individual neurons may behave.

==Mechanisms of activity==
As neurotoxins are compounds which adversely affect the nervous system, a number of mechanisms through which they function are through the inhibition of neuron cellular processes. These inhibited processes can range from membrane depolarization mechanisms to [[synapse|inter-neuron communication]]. By inhibiting the ability for neurons to perform their expected intracellular functions, or pass a signal to a neighboring cell, neurotoxins can induce systemic nervous system arrest as in the case of [[botulinum toxin]],<ref name=Arnon2001 /> or even nervous tissue death.<ref name=Brocardo2011>Brocardo 2011</ref> The time required for the onset of symptoms upon neurotoxin exposure can vary between different toxins, being on the order of hours for botulinum toxin<ref name=Thyagarajan2009 /> and years for lead.<ref>Lewendon 2001</ref>

{|| class="wikitable"
|-
! Neurotoxin classification
! Neurotoxins
|-
|Na channel inhibitors
|[[Tetrodotoxin]]<ref name=Kiernan2005>Kiernan 2005</ref>
|-
|K channel inhibitors
|[[Tetraethylammonium]]<ref name="Haghdoost-Yazdi2011">Haghdoost-Yazdi 2011</ref>
|-
|Cl channel inhibitors
|[[Chlorotoxin]],<ref name=DeBin1993>DeBin 1993</ref> 
|-
|Ca channel inhibitors
|[[Conotoxin]]<ref name=McClesky1987>McClesky 1987</ref>
|-
|Inhibitors of synaptic vesicle release
|[[Botulinum toxin]],<ref name="Garcia-Rodriguez2011">Garcia-Rodriguez 2011</ref> 

[[Tetanus|Tetanus toxin]]<ref name=Williamson1996>Williamson 1996</ref>
|-
|Blood brain barrier inhibitors
|[[Aluminium (element)|Aluminium]],<ref name=Banks1988 />

[[Mercury (element)|Mercury]]<ref name=Aschner1990>Aschner 1990</ref> 
|-
|Receptor inhibitors/antagonists
|[[Bungarotoxin]],<ref name=Dutertre2006>Dutertre 2006</ref>

[[Curare]]<ref name=Koller1988>Koller 1988</ref>
|-
|Receptor agonists
|[[Anatoxin-a]],<ref name=Carmichael1978 /><ref name=Carmichael1975 />

[[Caramboxin]],<ref name=Garcia-Cairasco2013 /> 

[[25I-NBOMe]],<ref name=Rutgrere2012>Rutgrere 2012</ref> 

[[JWH-018]],<ref name=Roller1994>Roller 1994</ref> 

[[5-MEO-DiPT]]
|-
|Cytoskeleton interference
|[[Ammonia]],<ref name=Konopacka2009>Konopacka 2009</ref>

[[Arsenic]]<ref name=DeFuria2006>DeFuria 2006</ref> 
|-
|Ca-mediated cytotoxicity
|[[Lead]]<ref name=Bressler1999>Bressler 1999</ref>
|-
|Protein misfolding
|[[Tau protein]]
|-
|Multiple effects
|[[Ethanol]],<ref name=Lovinger1989>{{cite journal | last1 = Lovinger | first1 = D. | last2 = White | first2 = G. | last3 = Weight | first3 = F. | year = 1989| title = Ethanol Inhibits NMDA-activated Ion Current in Hippocampal Neurons | url = https://zenodo.org/record/1230996| journal = Science | volume = 243 | issue = 4899| pages = 1721–724 | doi=10.1126/science.2467382| pmid = 2467382 | bibcode = 1989Sci...243.1721L }}</ref><ref name=Leonard1986>{{cite journal | last1 = Leonard | first1 = B. E. | year = 1986 | title = Is Ethanol a Neurotoxin?: the Effects of Ethanol on Neuronal Structure and Function | journal = Alcohol and Alcoholism | volume = 21 | issue = 4| pages = 325–38 | doi = 10.1093/oxfordjournals.alcalc.a044638 | pmid = 2434114 }}</ref>

[[N-Hexane]],<ref name=oshahexane />

[[Methanol]]<ref name=Lovinger1989 /><ref name=Leonard1986 />
|-
|Receptor-selective neurotoxins
|[[MPP+|MPP<sup>+</sup>]]
|-
|Endogenous neurotoxin sources
|[[Nitric oxide]],<ref name=Garthwaite1988>Garthwaite 1988</ref> 

[[Glutamate]],<ref name=Choi1990>Choi 1990</ref> 

[[Dopamine]]<ref name=BenShachar1995>{{cite journal |pmid=7830065 | volume=64 | issue=2 | title=Dopamine neurotoxicity: inhibition of mitochondrial respiration | year=1995 | journal=J. Neurochem. | pages=718–23 |vauthors=Ben-Shachar D, Zuk R, Glinka Y | doi = 10.1046/j.1471-4159.1995.64020718.x| s2cid=9060404 }}</ref>
|}

===Inhibitors===

====Sodium channel====

=====Tetrodotoxin=====
[[File:Puffer Fish DSC01257.JPG|thumb|alt=Puffer Fish.|The [[puffer fish]] is known for carrying lethal amounts of tetrodotoxin.]]

[[Tetrodotoxin]] (TTX) is a poison produced by organisms belonging to the [[Tetraodontiformes|Tetraodontiformes order]], which includes the [[puffer fish]], [[Molidae|ocean sunfish]], and [[porcupine fish]].<ref name=Chowdhury2007>{{cite journal | last1 = Chowdhury | first1 = F. R. | last2 = Ahasan | first2 = H A M. Nazmul | last3 = Rashid | first3 = A K M. Mamunur | last4 = Mamun | first4 = A. Al | last5 = Khaliduzzaman | first5 = S. M. | year = 2007 | title = Tetrodotoxin Poisoning: a Clinical Analysis, Role of Neostigmine and Short-term Outcome of 53 Cases | journal = Singapore Medical Journal | volume = 48 | issue = 9| pages = 830–33 | pmid = 17728964 }}</ref> Within the puffer fish, TTX is found in the [[liver]], [[gonads]], [[intestines]], and [[skin]].<ref name=Kiernan2005 /><ref>Ahasan 2004</ref> TTX can be fatal if consumed, and has become a common form of poisoning in many countries. Common symptoms of TTX consumption include [[paraesthesia]] (often restricted to the [[mouth]] and [[limb (anatomy)|limbs]]), muscle weakness, [[nausea]], and [[vomiting]]<ref name=Chowdhury2007 /> and often manifest within 30 minutes of [[ingestion]].<ref>Lau 1995</ref> The primary mechanism by which TTX is toxic is through the inhibition of sodium channel function, which reduces the functional capacity of neuron communication. This inhibition largely affects a susceptible subset of sodium channels known as TTX-sensitive (TTX-s), which also happens to be largely responsible for the sodium current that drives the [[depolarization|depolarization phase]] of neuron [[action potential]]s.<ref name=Kiernan2005 /> [[File:Tetrodotoxin AP.png|thumb|left|class=skin-invert-image|alt=Inhibited signaling in tetrodotoxin poisoning.|Inhibited signaling response resulting from neuron exposure to tetrodotoxin.]] TTX-resistant (TTX-r) is another form of sodium channel which has limited sensitivity to TTX, and is largely found in [[axon|small diameter axons]] such as those found in [[nociceptor|nociception neurons]].<ref name=Kiernan2005 /> When a significant level of TTX is ingested, it will bind sodium channels on neurons and reduce their [[membrane permeability]] to sodium. This results in an increased effective threshold of required excitatory signals in order to induce an action potential in a postsynaptic neuron.<ref name=Kiernan2005 /> The effect of this increased [[action potential|signaling threshold]] is a reduced excitability of [[chemical synapse|postsynaptic neurons]], and subsequent loss of motor and sensory function which can result in paralysis and death. Though [[medical ventilator|assisted ventilation]] may increase the chance of survival after TTX exposure, there is currently no antitoxin. The use of the acetylcholinesterase inhibitor [[Neostigmine]] or the muscarinic [[acetylcholine antagonist]] [[atropine]] (which will inhibit parasympathetic activity), however, can increase [[sympathetic nervous system|sympathetic nerve activity]] enough to improve the chance of survival after TTX exposure.<ref name=Chowdhury2007 />

====Potassium channel====

=====Tetraethylammonium=====
[[Tetraethylammonium]] (TEA) is a compound that, like a number of neurotoxins, was first identified through its damaging effects to the nervous system and shown to have the capacity of inhibiting the function of motor nerves and thus the contraction of the [[muscular system|musculature]] in a manner similar to that of curare.<ref name=Standfield1983>Standfield 1983</ref> Additionally, through chronic TEA administration, muscular atrophy would be induced.<ref name=Standfield1983 /> It was later determined that TEA functions in-vivo primarily through its ability to inhibit both the potassium channels responsible for the [[delayed rectifier outward potassium current|delayed rectifier]] seen in an [[action potential]] and some population of calcium-dependent potassium channels.<ref name="Haghdoost-Yazdi2011" /> It is this capability to inhibit potassium flux in neurons that has made TEA one of the most important tools in neuroscience. It has been hypothesized that the ability for TEA to inhibit potassium channels is derived from its similar space-filling structure to potassium ions.<ref name=Standfield1983 /> What makes TEA very useful for [[neuroscientist]]s is its specific ability to eliminate potassium channel activity, thereby allowing the study of neuron response contributions of other ion channels such as voltage gated sodium channels.<ref>Roed 1989</ref> In addition to its many uses in neuroscience research, TEA has been shown to perform as an effective treatment of [[Parkinson's disease]] through its ability to limit the progression of the disease.<ref>Haghdoost-Yasdi 2011</ref>

====Chloride channel====

=====Chlorotoxin=====
[[Chlorotoxin]] (Cltx) is the active compound found in [[scorpion]] venom, and is primarily toxic because of its ability to inhibit the conductance of [[chloride channel]]s.<ref name=DeBin1993 /> Ingestion of lethal volumes of Cltx results in paralysis through this ion channel disruption. Similar to botulinum toxin, Cltx has been shown to possess significant therapeutic value. Evidence has shown that Cltx can inhibit the ability for [[glioma]]s to infiltrate healthy nervous tissue in the brain, significantly reducing the potential invasive harm caused by tumors.<ref>Deshane 2003</ref><ref>Soroceanu 1998</ref>

====Calcium channel====

=====Conotoxin=====
[[Conotoxin]]s represent a category of poisons produced by the marine cone snail, and are capable of inhibiting the activity of a number of ion channels such as calcium, sodium, or potassium channels.<ref name=Jacob2010>Jacob 2010</ref><ref>Olivera 1987</ref> In many cases, the toxins released by the different types of [[Coninae|cone snails]] include a range of different types of conotoxins, which may be specific for different ion channels, thus creating a venom capable of widespread nerve function interruption.<ref name=Jacob2010 /> One of the unique forms of conotoxins, ω-conotoxin ([[conotoxin|ω-CgTx]]) is highly specific for Ca channels and has shown usefulness in isolating them from a system.<ref>Cruz 1986</ref> As calcium flux is necessary for proper excitability of a cell, any significant inhibition could prevent a large amount of functionality. Significantly, ω-CgTx is capable of long term binding to and inhibition of voltage-dependent calcium channels located in the membranes of neurons but not those of muscle cells.<ref>McCleskey 1987</ref>

====Synaptic vesicle release====

=====Botulinum toxin=====
[[File:Botulinum Toxin Mechanism.png|thumb|alt=Mechanism of Botulinum Toxin neurotoxicity.|Mechanism of Botulinum Toxin neurotoxicity]] [[Botulinum toxin]] (BTX) is a group of neurotoxins consisting of eight distinct compounds, referred to as BTX-A,B,C,D,E,F,G,H, which are produced by the bacterium ''[[Clostridium botulinum]]'' and lead to muscular [[paralysis]].<ref name=Brin1998>Brin, Mitchell F (1997) "Botulinum Toxin: Chemistry, Pharmacology, Toxicity, and Immunology." ''Muscle & Nerve,'' '''20''' (S6): 146–68.</ref> A notably unique feature of BTX is its relatively common therapeutic use in treating [[dystonia]] and [[spasticity]] disorders,<ref name=Brin1998 /> as well as in inducing [[muscular atrophy]]<ref name=Rosales1996 /> despite being the most poisonous substance known.<ref name=Thyagarajan2009 /> BTX functions peripherally to inhibit [[acetylcholine]] (ACh) release at the [[neuromuscular junction]] through degradation of the [[SNARE proteins]] required for ACh [[vesicle (biology and chemistry)|vesicle-membrane fusion]].<ref name="Garcia-Rodriguez2011" /> As the toxin is highly biologically active, an estimated dose of 1μg/kg body weight is sufficient to induce an insufficient tidal volume and resultant [[death]] by [[asphyxiation]].<ref name=Arnon2001 /> Due to its high toxicity, BTX antitoxins have been an active area of research. It has been shown that [[capsaicin]] (active compound responsible for heat in [[chili pepper]]s) can bind the [[TRPV1|TRPV1 receptor]] expressed on [[cholinergic|cholinergic neurons]] and inhibit the toxic effects of BTX.<ref name=Thyagarajan2009 />

=====Tetanus toxin=====
[[Tetanus|Tetanus neurotoxin]] (TeNT)  is a compound that functionally reduces inhibitory transmissions in the nervous system resulting in muscular tetany. TeNT is similar to BTX, and is in fact highly similar in structure and origin; both belonging to the same category of [[clostridium tetani|clostridial neurotoxins]].<ref name="Simpson1986" /> Like BTX, TeNT inhibits inter-neuron communication by means of vesicular neurotransmitter (NT) release.<ref name="Williamson1996" /> One notable difference between the two compounds is that while BTX inhibits [[muscle|muscular contractions]], TeNT induces them. Though both toxins inhibit vesicle release at neuron synapses, the reason for this different manifestation is that BTX functions mainly in the peripheral nervous system (PNS) while TeNT is largely active in the [[central nervous system]] (CNS).<ref>Montecucco 1986</ref> This is a result of TeNT migration through [[motor neuron]]s to the [[inhibitory neurotransmitter|inhibitory neurons]] of the spinal cord after entering through [[endocytosis]].<ref name="Pirazzini2011">Pirazzini 2011</ref> This results in a loss of function in inhibitory neurons within the CNS resulting in systemic [[muscle contraction|muscular contractions]]. Similar to the [[prognosis]] of a lethal dose of BTX, TeNT leads to paralysis and subsequent [[suffocation]].<ref name="Pirazzini2011" />

====Blood brain barrier====

=====Aluminium=====
Neurotoxic behavior of [[aluminium (element)|Aluminium]] is known to occur upon entry into the [[circulatory system]], where it can migrate to the brain and inhibit some of the crucial functions of the blood brain barrier (BBB).<ref name=Banks1988>Banks 1988</ref> A loss of function in the BBB can produce significant damage to the neurons in the CNS, as the barrier protecting the brain from other toxins found in the blood will no longer be capable of such action. Though the [[metal]] is known to be neurotoxic, effects are usually restricted to [[patient]]s incapable of removing excess ions from the blood, such as those experiencing [[renal failure]].<ref>King 1981</ref> Patients experiencing aluminium toxicity can exhibit [[symptom]]s such as impaired learning and reduced [[motor coordination]].<ref>Rabe 1982</ref> Additionally, systemic aluminium levels are known to increase with age, and have been shown to correlate with [[Alzheimer's disease]], implicating it as a neurotoxic causative compound of the disease.<ref>Walton 2006</ref> Despite its known toxicity in its ionic form, studies are divided on the potential toxicity of using aluminium in packaging and cooking appliances.

=====Mercury=====
[[Mercury (element)|Mercury]] is capable of inducing CNS damage by migrating into the brain by crossing the BBB.<ref name=Aschner1990 /> Mercury exists in a number of different compounds, though [[methylmercury]] (MeHg{{sup|+}}), [[dimethylmercury]] and [[diethylmercury]] are the only significantly neurotoxic forms. Diethylmercury and dimethylmercury are considered some of the most potent neurotoxins ever discovered.<ref name=Aschner1990 /> MeHg{{sup|+}} is usually acquired through consumption of [[seafood]], as it tends to concentrate in organisms high on the food chain.<ref>Chan 2011</ref> It is known that the mercuric ion inhibits [[amino acid]] (AA) and [[glutamate]] (Glu) transport, potentially leading to excitotoxic effects.<ref>Brookes 1988</ref>

===Receptor agonists and antagonists===

====Anatoxin-a====
{{External media
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 |video1=[http://www.periodicvideos.com/videos/mv_veryfastdeathfactor.htm Very Fast Death Factor]<br />University of Nottingham
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[[File:Anatoxin-a.svg|thumb|140px|right|class=skin-invert-image|[[Anatoxin-a|Anatoxin-''a'']]]]
Investigations into [[Anatoxin-a|anatoxin-''a'']], also known as "Very Fast Death Factor", began in 1961 following the deaths of cows that drank from a lake containing an [[algal bloom]] in Saskatchewan, Canada.<ref name=Carmichael1978>Carmichael 1978</ref><ref name=Carmichael1975>Carmichael 1975</ref> It is a [[cyanotoxin]] produced by at least four different genera of [[cyanobacteria]], and has been reported in North America, Europe, Africa, Asia, and New Zealand.<ref>Yang 2007</ref>

Toxic effects from anatoxin-''a'' progress very rapidly because it acts directly on the nerve cells ([[neuron]]s). The progressive symptoms of anatoxin-''a'' exposure are loss of coordination, [[Fasciculation|twitching]], convulsions and rapid death by [[respiratory paralysis]]. The nerve tissues which communicate with muscles contain a [[Receptor (biochemistry)|receptor]] called the [[nicotinic acetylcholine receptor]]. Stimulation of these receptors causes a [[muscular contraction]]. The anatoxin-''a'' molecule is shaped so it fits this receptor, and in this way it mimics the natural [[neurotransmitter]] normally used by the receptor, [[acetylcholine]]. Once it has triggered a contraction, anatoxin-''a'' does not allow the neurons to return to their resting state, because it is not degraded by [[cholinesterase]] which normally performs this function. As a result, the muscle cells contract permanently, the communication between the brain and the muscles is disrupted and breathing stops.<ref>Wood 2007</ref><ref>National Center for Environmental Assessment</ref>

When it was first discovered, the toxin was called the Very Fast Death Factor (VFDF) because when it was [[Intraperitoneal injection|injected into the body cavity]] of mice it induced tremors, paralysis and death within a few minutes. In 1977, the structure of VFDF was determined as a secondary, bicyclic [[amine]] [[alkaloid]], and it was renamed anatoxin-''a''.<ref>Devlin 1977</ref><ref>Moore 1977</ref> Structurally, it is similar to cocaine.<ref name=Metcalf>Metcalf 2009</ref> There is continued interest in anatoxin-''a'' because of the dangers it presents to recreational and drinking waters, and because it is a particularly useful molecule for investigating acetylcholine receptors in the nervous system.<ref name=Stewartetal>Stewart 2008</ref> The deadliness of the toxin means that it has a high military potential as a toxin weapon.<ref name=Dixitetal>Dixit 2005</ref>

====Bungarotoxin====
[[Bungarotoxin]] is a compound with known interaction with [[nicotinic acetylcholine receptor]]s (nAChRs), which constitute a family of [[ion channel]]s whose activity is triggered by neurotransmitter binding.<ref name=Tsetlin2003>Tsetlin 2003</ref> Bungarotoxin is produced in a number of different forms, though one of the commonly used forms is the long chain alpha form, [[α-bungarotoxin]], which is isolated from the [[banded krait|banded krait snake]].<ref name=Dutertre2006 /> Though extremely toxic if ingested, α-bungarotoxin has shown extensive usefulness in neuroscience as it is particularly adept at isolating nAChRs due to its high affinity to the receptors.<ref name=Dutertre2006 /> As there are multiple forms of bungarotoxin, there are different forms of nAChRs to which they will bind, and α-bungarotoxin is particularly specific for [[alpha-7 nicotinic receptor|α7-nAChR]].<ref name=Liu2008>Liu 2008</ref> This α7-nAChR functions to allow [[calcium ion]] influx into cells, and thus when blocked by ingested bungarotoxin will produce damaging effects, as ACh signaling will be inhibited.<ref name=Liu2008 /> Likewise, the use of α-bungarotoxin can be very useful in neuroscience if it is desirable to block calcium flux in order to isolate effects of other channels. Additionally, different forms of bungarotoxin may be useful for studying inhibited nAChRs and their resultant calcium ion flow in different systems of the body. For example, α-bungarotoxin is specific for nAChRs found in the musculature and [[κ-bungarotoxin]] is specific for nAChRs found in neurons.<ref>Hue 2007</ref>

=====Caramboxin=====
[[File:Caramboxin.svg|thumb|140px|right|class=skin-invert-image|[[Caramboxin]]]]
[[Caramboxin]] (CBX) is a [[toxin]] found in [[star fruit]] (''Averrhoa carambola)''. Individuals with some types of kidney disease are susceptible to adverse neurological effects including intoxication, seizures and even death after eating star fruit or drinking juice made of this fruit.  Caramboxin is a new nonpeptide amino acid toxin that stimulate the glutamate receptors in neurons. Caramboxin is an agonist of both [[NMDA receptor|NMDA]] and [[AMPA receptor|AMPA]] glutamatergic ionotropic receptors with potent excitatory, convulsant, and neurodegenerative properties.<ref name=Garcia-Cairasco2013>{{Cite journal | last1 = Garcia-Cairasco | first1 = N. | last2 = Moyses-Neto | first2 = M. | last3 = Del Vecchio | first3 = F. | last4 = Oliveira | first4 = J. A. C. | last5 = Dos Santos | first5 = F. L. | last6 = Castro | first6 = O. W. | last7 = Arisi | first7 = G. M. | last8 = Dantas | first8 = M. R. | last9 = Carolino | first9 = R. O. G. | last10 = Coutinho-Netto | first10 = J. | last11 = Dagostin | first11 = A. L. A. | last12 = Rodrigues | first12 = M. C. A. | last13 = Leão | first13 = R. M. | last14 = Quintiliano | first14 = S. A. P. | last15 = Silva | first15 = L. F. | last16 = Gobbo-Neto | first16 = L. | last17 = Lopes | first17 = N. P. | title = Elucidating the Neurotoxicity of the Star Fruit | doi = 10.1002/anie.201305382 | journal = Angewandte Chemie International Edition | volume = 52 | issue = 49 | pages = 13067–13070 | year = 2013 | pmid =  24281890}}</ref>

=====Curare=====
The term "[[curare]]" is ambiguous because it has been used to describe a number of poisons which at the time of naming were understood differently from present day understandings. In the past the characterization has meant poisons used by [[indigenous peoples of the americas|South American tribes]] on [[arrow]]s or [[dart (missile)|darts]], though it has matured to specify a specific categorization of poisons which act on the [[neuromuscular junction]] to inhibit signaling and thus induce muscle relaxation.<ref name="Bisset1992">Bisset 1992</ref> The neurotoxin category contains a number of distinct poisons, though all were originally purified from plants originating in South America.<ref name="Bisset1992" /> The effect with which injected curare poison is usually associated is muscle paralysis and resultant death.<ref name=Schlesinger1946>Schlesinger 1946</ref> Curare notably functions to inhibit [[nicotinic acetylcholine receptors]] at the [[neuromuscular junction]].  Normally, these receptor channels allow sodium ions into muscle cells to initiate an action potential that leads to muscle contraction.  By blocking the receptors, the neurotoxin is capable of significantly reducing neuromuscular junction signaling, an effect which has resulted in its use by [[anesthesiologists]] to produce muscular relaxation.<ref>{{cite journal | last1 = Griffith | first1 = Harold R. | last2 = Johnson | first2 = G. Enid | year = 1942 | title = The Use Of Curare In General Anesthesia | journal = Anesthesiology | volume = 3 | issue = 4| pages = 418–420 | doi=10.1097/00000542-194207000-00006| s2cid = 71400545 | doi-access = free }}</ref>

===Cytoskeleton interference===

==== Ammonia ====
[[File:Astrocyte endothel interaction 01.png|thumb|alt=Astrocyte.|An Astrocyte, a cell notable for maintaining the blood brain barrier]]

[[Ammonia]] toxicity is often seen through two routes of administration, either through consumption or through endogenous ailments such as [[liver failure]].<ref name=Matsuoka1991>Matsuoka 1991</ref><ref>Buzanska (2000)</ref> One notable case in which ammonia toxicity is common is in response to [[cirrhosis]] of the [[liver]] which results in [[hepatic encephalopathy]], and can result in [[cerebral edema]] (Haussinger 2006). This cerebral edema can be the result of nervous cell remodeling. As a consequence of increased concentrations, ammonia activity in-vivo has been shown to induce swelling of astrocytes in the brain through increased production of [[cyclic guanosine monophosphate|cGMP (Cyclic Guanosine Monophosphate)]] within the cells which leads to [[cGMP-dependent protein kinase|Protein Kinase G-mediated]] (PKG) cytoskeletal modifications.<ref name=Konopacka2009 /> The resultant effect of this toxicity can be reduced brain energy [[metabolism]] and function. Importantly, the toxic effects of ammonia on astrocyte remodeling can be reduced through administration of [[carnitine|L-carnitine]].<ref name=Matsuoka1991 /> This astrocyte remodeling appears to be mediated through ammonia-induced [[mitochondria]]l permeability transition. This mitochondrial transition is a direct result of [[glutamine]] activity a compound which forms from ammonia in-vivo.<ref name=Norenberg2004>Norenberg 2004</ref> Administration of [[antioxidant]]s or [[glutaminase]] inhibitor can reduce this mitochondrial transition, and potentially also astrocyte remodeling.<ref name=Norenberg2004 />

====Arsenic====
[[Arsenic]] is a neurotoxin commonly found concentrated in areas exposed to [[agricultural runoff]], [[mining]], and [[smelting]] sites (Martinez-Finley 2011). One of the effects of arsenic ingestion during the development of the nervous system is the inhibition of [[neurite]] growth<ref>Liu 2009{{full citation needed|date=October 2020}}</ref> which can occur both in PNS and the CNS.<ref>Vahidnia 2007</ref> This neurite growth inhibition can often lead to defects in [[neuronal migration|neural migration]], and significant morphological changes of neurons during [[developmental biology|development]],<ref name=Rocha2011>Rocha 2011</ref>) often leading to [[neural tube]] defects in [[infant|neonates]].<ref>Brender 2005</ref> As a [[metabolite]] of arsenic, [[arsenite]] is formed after ingestion of arsenic and has shown significant toxicity to neurons within about 24 hours of exposure. The mechanism of this cytotoxicity functions through arsenite-induced increases in [[intracellular]] calcium ion levels within neurons, which may subsequently reduce mitochondrial transmembrane potential which activates [[caspase]]s, triggering cell death.<ref name=Rocha2011 /> Another known function of arsenite is its destructive nature towards the [[cytoskeleton]] through inhibition of [[neurofilament]] transport.<ref name=DeFuria2006 /> This is particularly destructive as neurofilaments are used in basic cell structure and support. [[Lithium]] administration has shown promise, however, in restoring some of the lost neurofilament motility.<ref>DeFuria 2007</ref> Additionally, similar to other neurotoxin treatments, the administration of certain antioxidants has shown some promise in reducing neurotoxicity of ingested arsenic.<ref name=Rocha2011 />

===Calcium-mediated cytotoxicity===

====Lead====
[[File:Trinkwasserleitung Blei.jpg|thumb|alt=Lead Pipe.|Lead pipes and solder are common sources of ingested lead.]]

[[Lead]] is a potent neurotoxin whose toxicity has been recognized for at least thousands of years.<ref name=Lidskey2003>Lidskey 2003</ref> Though neurotoxic effects for lead are found in both [[adult]]s and young [[child]]ren, the developing brain is particularly susceptible to lead-induced harm, effects which can include [[apoptosis]] and excitotoxicity.<ref name=Lidskey2003 /> An underlying mechanism by which lead is able to cause harm is its ability to be transported by [[atpase|calcium ATPase pumps]] across the BBB, allowing for direct contact with the fragile cells within the central nervous system.<ref>Bradbury 1993</ref> Neurotoxicity results from lead's ability to act in a similar manner to calcium ions, as concentrated lead will lead to cellular uptake of calcium which disrupts cellular [[homeostasis]] and induces apoptosis.<ref name=Bressler1999 /> It is this intracellular calcium increase that activates [[protein kinase C]] (PKC), which manifests as learning deficits in children as a result of early lead exposure.<ref name=Bressler1999 /> In addition to inducing apoptosis, lead inhibits interneuron signaling through the disruption of calcium-mediated neurotransmitter release.<ref>Lasley 1999</ref>

===Neurotoxins with multiple effects===

====Ethanol====
[[File:Photo of baby with FAS.jpg|thumb|alt=Image of Fetal Alcohol Syndrome|Male baby exhibiting [[Fetal Alcohol Syndrome]] (FAS).]]

As a neurotoxin, [[ethanol]] has been shown to induce nervous system damage and affect the body in a variety of ways. Among the known effects of ethanol exposure are both transient and lasting consequences. Some of the lasting effects include long-term reduced [[neurogenesis]] in the [[hippocampus]],<ref>Taffe 2010</ref><ref>Morris 2009</ref> widespread brain atrophy,<ref>Bleich 2003</ref> and induced [[inflammation]] in the brain.<ref>Blanco 2005</ref> Of note, chronic ethanol ingestion has additionally been shown to induce reorganization of cellular membrane constituents, leading to a [[lipid bilayer]] marked by increased membrane concentrations of [[cholesterol]] and [[saturated fat]].<ref name=Leonard1986 /> This is important as neurotransmitter transport can be impaired through vesicular transport inhibition, resulting in diminished neural network function. One significant example of reduced inter-neuron communication is the ability for ethanol to inhibit [[nmda receptor|NMDA receptors]] in the hippocampus, resulting in reduced [[long-term potentiation]] (LTP) and memory acquisition.<ref name=Lovinger1989 /> NMDA has been shown to play an important role in LTP and consequently memory formation.<ref>Davis 1992</ref> With chronic ethanol intake, however, the susceptibility of these NMDA receptors to induce LTP increases in the [[mesolimbic pathway|mesolimbic dopamine neurons]] in an [[inositol triphosphate|inositol 1,4,5-triphosphate]] (IP3) dependent manner.<ref>Bernier 2011</ref> This reorganization may lead to neuronal cytotoxicity both through hyperactivation of postsynaptic neurons and through induced addiction to continuous ethanol consumption. It has, additionally, been shown that ethanol directly reduces intracellular calcium ion accumulation through inhibited NMDA receptor activity, and thus reduces the capacity for the occurrence of LTP.<ref name=Takadera1990>Takadera 1990</ref>

In addition to the neurotoxic effects of ethanol in mature organisms, chronic ingestion is capable of inducing severe developmental defects. Evidence was first shown in 1973 of a connection between chronic ethanol intake by mothers and defects in their offspring.<ref>Jones 1973</ref> This work was responsible for creating the classification of [[fetal alcohol syndrome]], a disease characterized by common [[morphogenesis]] aberrations such as defects in [[craniofacial]] formation, limb development, and [[cardiovascular system|cardiovascular]] formation. The magnitude of ethanol neurotoxicity in [[fetus]]es leading to fetal alcohol syndrome has been shown to be dependent on antioxidant levels in the brain such as [[vitamin e|vitamin E]].<ref>Mitchell 1999</ref> As the fetal brain is relatively fragile and susceptible to induced stresses, severe deleterious effects of alcohol exposure can be seen in important areas such as the hippocampus and [[cerebellum]]. The severity of these effects is directly dependent upon the amount and frequency of ethanol consumption by the mother, and the stage in development of the fetus.<ref>Gil-Mohapel 2010</ref> It is known that ethanol exposure results in reduced antioxidant levels, mitochondrial dysfunction (Chu 2007),  and subsequent neuronal death, seemingly as a result of increased generation of [[reactive oxygen species|reactive oxidative species]] (ROS).<ref name=Brocardo2011 /> This is a plausible mechanism, as there is a reduced presence in the fetal brain of antioxidant enzymes such as [[catalase]] and [[peroxidase]].<ref>Bergamini 2004</ref> In support of this mechanism, administration of high levels of [[diet (nutrition)|dietary]] vitamin E results in reduced or eliminated ethanol-induced neurotoxic effects in fetuses.<ref name=Heaton2000 />

====n-Hexane====

n-[[Hexane]] is a neurotoxin which has been responsible for the poisoning of several workers in Chinese electronics factories in recent years.<ref>[https://archive.today/20120716110552/http://www.abc.net.au/news/stories/2010/10/26/3048024.htm Workers poisoned while making iPhones] ABC News, October 25, 2010</ref><ref>[http://www.abc.net.au/foreign/content/2010/s3044840.htm Dirty Secrets] {{Webarchive|url=https://web.archive.org/web/20170525081658/http://www.abc.net.au/foreign/content/2010/s3044840.htm |date=2017-05-25 }} ABC Foreign Correspondent, 2010-Oct-26</ref><ref>[http://www.thisamericanlife.org/radio-archives/episode/454/mr-daisey-and-the-apple-factory Mr Daisey and the Apple Factory], This American Life, January 6, 2012</ref><ref name=oshahexane>[http://www.osha.gov/SLTC/healthguidelines/n-hexane/recognition.html Occupational Safety and Health Guideline for n-Hexane] {{webarchive|url=https://web.archive.org/web/20111218221317/http://www.osha.gov/SLTC/healthguidelines/n-hexane/recognition.html |date=2011-12-18 }}, OSHA.gov</ref>

===Receptor-selective neurotoxins===

====MPP<sup>+</sup>====
[[MPP+|MPP<sup>+</sup>]], the toxic metabolite of [[MPTP]] is a selective neurotoxin which interferes with [[oxidative phosphorylation]] in [[mitochondria]] by inhibiting [[complex I]], leading to the depletion of [[Adenosine triphosphate|ATP]] and subsequent cell death. This occurs almost exclusively in dopaminergic neurons of the [[substantia nigra]], resulting in the presentation of permanent [[parkinsonism]] in exposed subjects 2–3 days after administration.

===Endogenous neurotoxin sources===
Unlike most common sources of neurotoxins which are acquired by the body through ingestion, endogenous neurotoxins both originate from and exert their effects [[in vivo|in-vivo]]. Additionally, though most venoms and exogenous neurotoxins will rarely possess useful in-vivo capabilities, endogenous neurotoxins are commonly used by the body in useful and healthy ways, such as nitric oxide which is used in cell communication.<ref>Iadecola 1998</ref> It is often only when these endogenous compounds become highly concentrated that they lead to dangerous effects.<ref name=Choi1987 />

====Nitric oxide====
Though [[nitric oxide]] (NO) is commonly used by the nervous system in inter-neuron communication and signaling, it can be active in mechanisms leading to [[ischemia]] in the cerebrum (Iadecola 1998). The neurotoxicity of NO is based on its importance in glutamate excitotoxicity, as NO is generated in a calcium-dependent manner in response to glutamate mediated NMDA activation, which occurs at an elevated rate in glutamate excitotoxicity.<ref name=Garthwaite1988 /> Though NO facilitates increased blood flow to potentially ischemic regions of the brain, it is also capable of increasing [[oxidative stress]],<ref>Beckman 1990</ref> inducing DNA damage and apoptosis.<ref>Bonfoco 1995</ref> Thus an increased presence of NO in an ischemic area of the CNS can produce significantly toxic effects.

====Glutamate====
[[Glutamate]], like nitric oxide, is an endogenously produced compound used by neurons to perform normally, being present in small concentrations throughout the [[gray matter]] of the CNS.<ref name=Choi1987 /> One of the most notable uses of endogenous glutamate is its functionality as an excitatory neurotransmitter.<ref name=Choi1990 /> When concentrated, however, glutamate becomes toxic to surrounding neurons. This toxicity can be both a result of direct lethality of glutamate on neurons and a result of induced calcium flux into neurons leading to swelling and necrosis.<ref name=Choi1990 /> Support has been shown for these mechanisms playing significant roles in diseases and complications such as [[Huntington's disease]], [[epilepsy]], and [[stroke]].<ref name=Choi1987 />

==See also==
*[[Babycurus toxin 1]]
*[[Cangitoxin]]
*[[Chronic solvent-induced encephalopathy]]
*[[Fertilizer]]
*[[Herbicide]]
*[[Pesticides]]
*[[Solvent]]
*[[Toxic encephalopathy]]

==Notes==
{{reflist|15em}}

==References==
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{{refend}}

==Further reading==
*[https://web.archive.org/web/20120131032408/http://www.sfn.org/skins/main/pdf/brainfacts/2008/brain_facts.pdf Brain Facts Book] at The Society for Neuroscience
*[https://web.archive.org/web/20160214021422/http://neuroscience.uth.tmc.edu/ Neuroscience Texts] at University of Texas Medical School
*[https://doi.org/10.1007%2F978-1-61779-170-3_1 In Vitro Neurotoxicology: An Introduction] at Springerlink
*[https://www.ncbi.nlm.nih.gov/books/NBK5283/ Biology of the NMDA Receptor] at NCBI
*[https://www.ncbi.nlm.nih.gov/books/NBK53356/ Advances in the Neuroscience of Addiction, 2nd edition] at NCBI

==External links==
{{Wiktionary|neurotoxin}}
{{Commons category|Neurotoxins}}
*[http://www.epa.gov/ Environmental Protection Agency] at United States Environmental Protection Agency
*[https://web.archive.org/web/20050604001441/http://alcalc.oxfordjournals.org/ Alcohol and Alcoholism] at Oxford Medical Journals
*[https://web.archive.org/web/20091014044352/http://toxipedia.org/display/toxipedia/Neurotoxins Neurotoxins] at Toxipedia

{{Neurotoxins|state=expanded}}
{{Neuroscience}}
{{Toxins}}
{{Cyanotoxins}}

[[Category:Neurotoxins| ]]