Neurotoxins effect

In many papers neurotoxin effects on cells, synaptosomes or lipid vesicles containing purified channels were studied by means of Na+ uptake. Recently the intravesicular increase in Na" " concentration has also been monitored with fluorescent indicators (Daniell 1992 Deri and Adma-Vizi... 

Horn, A.S. Structure-Activity Relationships of Serotonin Neurotoxins Effects on Serotonin Uptake in Serotonin Neurotoxins (1978)... 

While neurotoxins effectively stop nerve and muscle function without causing microscopic damage to the tissues, membrane-damaging toxins destroy or damage tissue directly. For these toxins, prophylaxis is important, because the point at which the pathological change becomes irreversible often occurs within minutes to a few hours after exposure. 

Tetrodotoxin is one of the most powerful non-protein neurotoxins known. It occurs in the liver and ovaries of the Japanese puffer fish, Sphoerides rubripes and S. phyreus, and its lethal effects have been known for centuries, although it was isolated in crystalline form... 

Wild, JR USDA To develop an effective and complete biological remediation system capable of hydrolyzing organophosphorous neurotoxins from agricultural and chemical warfare munitions, contaminations, and wastes. 

From an ecotoxicological point of view, it has often been suspected that sublethal effects, such as those described here, can be more important than lethal ones. Both p,p -DDT and p,p -DDD are persistent neurotoxins, and may very well have caused behavioral effects in the field. This issue was not resolved when DDT was widely used, and remains a matter for speculation. More is known, however, about eggshell thinning caused by p,p -DDE and its effects upon reproduction, which will be discussed in Section 5.2.5.I. 

Recently, there has been a growth of interest in the development of in vitro methods for measuring toxic effects of chemicals on the central nervous system. One approach has been to conduct electrophysiological measurements on slices of the hippocampus and other brain tissues (Noraberg 2004, Kohling et al. 2005). An example of this approach is the extracellular recording of evoked potentials from neocortical slices of rodents and humans (Kohling et al. 2005). This method, which employs a three-dimensional microelectrode array, can demonstrate a loss of evoked potential after treatment of brain tissue with the neurotoxin trimethyltin. Apart from the potential of in vitro methods such as this as biomarkers, there is considerable interest in the use of them as alternative methods in the risk assessment of chemicals, a point that will be returned to in Section 16.8. 

Research in this area advanced in the 1970 s as several groups reported the isolation of potent toxins from P. brevis cell cultures (2-7). To date, the structures of at least eight active neurotoxins have been elucidated (PbTx-1 through PbTx-8) (8). Early studies of toxic fractions indicated diverse pathophysiological effects in vivo as well as in a number of nerve and muscle tissue preparations (reviewed in 9-11). The site of action of two major brevetoxins, PbTx-2 and PbTx-3, has been shown to be the voltage-sensitive sodium channel (8,12). These compounds bind to a specific receptor site on the channel complex where they cause persistent activation, increased Na flux, and subsequent depolarization of excitable cells at resting... 

While most investigations show that sea snake neurotoxins are postsynaptic type, Gawade and Gaitonde (23) stated that Enhydrina schistosa major toxin has dual actions or postsynaptic as well as presynaptic toxicity. E, schistosa venom phospholipase A is both neurotoxic and myotoxic. Neurotoxic action of the enzyme is weak so that there is sufficient time for myonecrotic action to take place (24), Sea snake, L. semifasciata toxin also inhibits transmission in autonomic ganglia, but has no effect on transmission in choroid neurons. 

The question is obviously an important one. Substances released from neurons are not always called neurotransmitters. Some of them are referred to as neuromodulators, neurohormones, neurotrophic factors or neurotoxins but since they all produce some effect on a neuron they could be said to have a transmitter role and justify the term... 

If excessive noradrenergic transmission is a causal factor in anxiety, then it would be predicted that a lesion of central noradrenergic neurons would have an anti-anxiety effect in behavioural models of this condition. Unfortunately, the behavioural effects of such lesions are notoriously inconsistent and there are many reports of negative findings (e.g. Salmon, Tsaltas and Gray 1989). One study has even shown that a lesion of central noradrenergic neurons, induced by the selective neurotoxin, DSP-4, abolishes the anti-anxiety effects of tricyclic antidepressants and MAO inhibitors, but not those of the benzodiazepine, alprazolam, or the barbiturate, phenobarbitone (Fontana,... 

ED35 Eflective dose producing 35% maximum response EDso Effective dose producing 50% maximum response EDF Eosinophil differentiation 6ctor EDL Extensor digitorum longus EDN Eosinophil-derived neurotoxin EDRF Endothelium-derived relaxing factor... 

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