Neurons are essential cells involved in the transmission of messages in the central nervous system (CNS) and peripheral nervous system (PNS). The transmission of the messages is accomplished by networks of neurons forming biological communication networks. Neurotoxins affect neurons, leading to their death or injury. Transected neurons are severed cells with altered chemical and structural ability to transmit impulses along the CNS or the PNS. They lack functional extensions like the axons and dendrites, and the myelin sheaths. It has been demonstrated that most neurotoxins affect the cell bodies of neurons in both the PNS and the CNS. However, some neurotoxins act on the axons of neurons, severing the myelin sheaths surrounding the extensions, but leaving cell bodies intact. In such cases, the neurotoxin leads to chemical transection of the axons. Such axons become biologically isolated from the cell body of the neuron. Research demonstrates that chemically transected axons of the PNS can regenerate while those of the CNS cannot regenerate. Different chemicals have different modes through which chemical transection of neurons is initiated.
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DDT is an organochloride neurotoxin that alters the rate at which potassium ions get into neurons. It also affects the active transport of sodium ions out neurons when they are repolarized. The organochloride inhibits Na+, K+ and Ca2+ ATPase when neurons are repolarized. These actions of the neurotoxin result in prolonged negative phase in the action of the stimuli. The repetitive stimulation in the PNS is further amplified in the CNS, resulting in continuous tremor in the poisoned individual.
Organophosphorous pesticide effects are produced by inhibition of the enzyme acetylcholinesterase, which hydrolyzes acetylcholine. When the enzyme is inhibited, there is prolonged stimulation in cholinergic nerves by the neurotransmitter acetylcholine. Prolonged stimulation of the muscarinic nerve endings leads to hyperactivity of multiple responses in the parasympathetic nervous system. Prolonged action of acetylcholine also causes neurons within the sympathetic and parasympathetic nervous system to be depolarized.
Organophosphates have been implicated in delayed neuropathy resulting several days after the initial exposure. The delayed neuropathy has been attributed to demyelination of axons and phosphorylation of esterase in neurons. However, acetylcholinesterase and paraoxon do not produce delayed neuropathy.
Carbon disulfide induces axonopathies by interfering with transport of chemicals along axons. The interference is achieved by linking filaments within axons via covalent bonds. Acrylamide is another neurotoxin that has been shown to cause axonopathies, beginning at the terminals of axons and proceeding proximally. There is controversy on the exact mode of action, but several studies support the idea that impaired transport along axons is involved. Organic lead has been confirmed to cause myelinopathies which are characterized by chronic exposures. The myelinopathies produced by organic lead mostly affect motor neurons rather than the sensory neurons. Hexachlorophene also induces myelinopathies by oxidative phosphorylation within neurons, affecting the myelin sheaths of the axons. The compound is rapidly absorbed by human skin, and it affects both the CNS and PNS. One of the most common effects of this neurotoxin is edema in the central nervous system and peripheral nervous system. Myelinopathies lead to altered conduction of impulses along nerves. The properties of the alteration produced may be decreased speed of action potential, blockage or irregular transmission. It has also been shown that axonopathies mostly affect long axons of the central nervous system and peripheral nervous system.