Nerve cells, damage

Neurotrophic factors are chemical substances secreted by target post-synap-tic cells into synaptic clefts. They are taken up by the pre-synaptic terminal and transported retrogradely along the axon to the cell-body where they modify neuronal metabolism, often by affecting protein synthesis. Experimental blockade of neurotrophic factors results in nerve cell damage or death. 

Fig. 120.4 Mechanism of oxidative damage on nerve cell. Damage can be prevented in two ways (1) by prevaiting formation of ROS or (2) by scavenging ROS...

This is in contradistinction to the situation in MeHg-intoxicated children or adults, in which neurons within specific regions are affected more or less selectively. The effects upon neurons during earlier phases of development may not be readily apparent on examination of neonatal brains because of the difficulty in identifying the sites of nerve cell damage or loss in the absence of vigorous cellular (i.e., macrophage or astrocyte) response. 

Note S Precaution—n-Hexane is extremely flammable, harmful if inhaled, may produce nerve cell damage see Annex A 1.1. 

Note 4—Warning Extremely flammable. Harmful if inhaled. May produce nerve cell damage. Vapors may cause flash fire. 

There are as many incidents of poisoning by OPPs as there are by OCPs [12, 40, 46, A8]. All OPPs are polytropic poisons. Changes are observed in the brain nerve cells of victims of acute OPP poisoning. Acute poisoning accompanied by diffuse damage to the central nervous system causes attacks similar to epileptic fits when symptoms of clinical poisoning have already... 

Other people thought the opposite that some of the LSD is sequestered in the brain for extended periods, possibly providing an explanation for flashbacks. Some believed that these small amounts of residual LSD could also cause brain damage. Additional research has fairly well refuted both beliefs. The possibility remains, however, that subtle changes at the sub-microscopic level, perhaps involving specific enzymes within nerve cells, might result from... 

Stopping Neurotransmission. Turning off the neurotransmitter signal once it has been released into the synapse is critical to successful communication between nerve cells. This is of paramount importance because unbridled stimulation can be harmful to nerve cells. For example, one of the problems in the minutes and hours following a stroke is that nerve cells near the stroke area can literally be stimulated to death. In fact, some of the new medications used to minimize damage to the brain after a stroke act by literally calming the cells in the brain. Thus, signal termination is a critically important aspect of neurotransmission. 

Too Little Neurotransmission. In some cases, disease appears to damage or cause the death of nerve cells, a process called neurodegeneration. These diseases cause problems by stopping normal neurotransmission altogether. One example of this disease process is Alzheimer s disease, the major cause of dementia in the elderly. In this common and devastating illness, acetylcholine-containing nerve cells, and others, die prematurely. 

Why don t any of these medications work Clearly, they boost nerve cell activity. Some of them do enhance cognition in animals. But they do little for dementia patients. Why is this The explanation is probably that the small benefit of these medications pales in comparison to the widespread damage to nerve cells caused by dementia. The difference between a dementia s ability to compromise the way the brain works and a medication s ability to enhance brain function is so great that the medication produces no noticeable improvement. 

Most of the other medications studied to slow the course of Alzheimer s dementia presumably work as an antioxidant to protect nerve cells from damaging free radicals. Of the antioxidants, vitamin E is the safest and has the best evidence of efficacy. Thus, we recommend that all patients receive 2000 lU of vitamin E each day during... 

After exposure to high levels of carbon tetrachloride, the nervous system, including the brain, is affected. Such exposure can be fatal. The immediate effects are usually signs of intoxication, including headache, dizziness, and sleepiness perhaps accompanied by nausea and vomiting. These effects usually disappear within a day or two after exposure stops. In severe cases, stupor or even coma can result, and permanent damage to nerve cells can occur. 

The cell damage associated with inflammation acts on cell membranes to cause leukocytes to release lysosomal enzymes arachidonic acid is then liberated from precursor compounds, and various eicosanoids are synthesized. As discussed in Chapter 18, the cyclooxygenase (COX) pathway of arachidonate metabolism produces prostaglandins, which have a variety of effects on blood vessels, on nerve endings, and on cells involved in inflammation. The lipoxygenase pathway of arachidonate metabolism yields leukotrienes, which have a powerful chemotactic effect on eosinophils, neutrophils, and macrophages and promote bronchoconstriction and alterations in vascular permeability. 

Hydroxy dopamine is a selectively neuro toxic compound, which damages the sympathetic nerve endings. It can be seen from Figure 7.43 that 6-hydroxydopamine is structurally very similar to dopamine and noradrenaline, and because of this similarity it is actively taken up into the synaptic system along with other catecholamines. Once localized in the synapse, the 6-hydroxydopamine destroys the nerve terminal. A single small dose of 6-hydroxydopamine destroys all the nerve terminals and possibly the nerve cells as well. 

The toxic effect is known as histotoxic hypoxia. Cyanide also directly stimulates chemoreceptors, causing hyperpnea. Lack of ATP will affect all cells, but heart muscle and brain are particularly susceptible. Therefore, cardiac arrythmias and other changes often occur, resulting in circulatory failure and delayed tissue ischemic anoxia. Death is usually due to respiratory arrest resulting from damage to the CNS, as the nerve cells of the respiratory control center are particularly sensitive to hypoxia. The susceptibility of the brain to pathological damage may reflect the lower concentration of cytochrome oxidase in white matter. 

This selectively neurotoxic compound damages the sympathetic nerve endings. Because of its structural similarity to dopamine, it is actively taken up into the synaptic system. Once taken up, it oxidizes to a reactive quinone, which may bind to protein and produce reactive free radicals and superoxide. These events destroy the nerve terminals and nerve cells also in some cases. 

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