exposure. in addition to inducing apoptosis, lead inhibits interneuron signaling through the disruption of calcium-mediated neurotransmitter release. ethanol 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, widespread brain atrophy, and induced inflammation in the brain. 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. 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 receptors in the hippocampus, resulting in reduced long-term potentiation (ltp) and memory acquisition. nmda has been shown to play an important role in ltp and consequently memory formation. with chronic ethanol intake, however, the susceptibility of these nmda receptors to induce ltp increases in the mesolimbic dopamine neurons in an inositol 1,4,5-triphosphate (ip3) dependent manner. 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. 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. 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 formation. the magnitude of ethanol neurotoxicity in fetuses leading to fetal alcohol syndrome has been shown to be dependent on antioxidant levels in the brain such as vitamin e. 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. 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 oxidative species (ros). this is a plausible mechanism, as there is a reduced presence in the fetal brain of antioxidant enzymes such as catalase and peroxidase. in support of this mechanism, administration of high levels of dietary vitamin e results in reduced or eliminated ethanol-induced neurotoxic effects in fetuses. n-hexane n-hexane is a neurotoxin which has been responsible for the poisoning of several workers in chinese electronics factories in recent years. mpp+ mpp+, 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 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. 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. it is often only when these endogenous compounds become highly concentrated that they lead to dangerous effects. 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. though no facilitates increased blood flow to potentially ischemic regions of the brain, it is also capable of increasing oxidative stress, inducing dna damage and apoptosis. 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. one of the most notable uses of endogenous glutamate is its functionality as an excitatory neurotransmitter. 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. support has been shown for these mechanisms playing significant roles in diseases and complications such as huntington's disease, epilepsy, and stroke.