Titlebook: Selective Neurotoxicity; Hans Herken,Ferdinand Hucho Book 1992 Springer-Verlag Berlin Heidelberg 1992 Calcium.Glutamat.Nucleotide.dopamine

窒息

Tetanus and Botulinum Neurotoxins,ture, they are translocated into neurons by adsorptive endocytosis, and they act predominantly on nerve cells. They have so many features in common (. H. 1982; M. 1984; S. 1990) that a comparative discussion not only appears to be justified but may contribute to a better understanding of the whole g

创新

Capsaicin: Selective Toxicity for Thin Primary Sensory Neurons,lyl-6-nonenamide (Fig. 1) with a molecular weight of 305.42. It was only by the middle of this century that N. Jancso realized that capsaicin, in addition to its irritant effect, has a long-term sensory neuron-blocking action which can be used in the functional investigation of sensory neurons (J. 1

极小量

Excitotoxins, Glutamate Receptors, and Excitotoxicity,inclusion of a chapter on excitotoxins and Glu receptors in a book devoted to neurotoxins. Recent reviews dealing with the topic are available particularly with regard to the involvement of Glu and Glu receptors in CNS ontogeny (M.D. and J. 1990), physiology (C. and L. 1989), and pathology (C. and R

寄生虫

Convulsants and Gamma-Aminobutyric Acid Receptors,ally important disorders (B. et al. 1985), including epilepsy (G. 1989). The complexity of neuronal integration in the brain has precluded any detailed understanding of these conditions, though much information has been gleaned from the consequences of intervention with a variety of pharmacological

Banquet

熔岩

Peptide Toxins Acting on the Nicotinic Acetylcholine Receptor,he focus of interest for researchers investigating the mechanisms of propagation and transmission of nerve impulses. Neurotoxins turned out to be very valuable tools in these investigations (M. and H. 1990; H. and O. 1983). They are currently used for elucidating the proteins of nerve and muscle mem

男学院

散步

同位素

Peptide Toxins that Alter Neurotransmitter Release, mechanism(s) involved (V. et al. 1990; T. and P. 1991). Clearly, progress with this challenging problem ought to be achieved by identifying molecular components in nerve terminals concerned with the process or its regulation. As several neurotoxins have been characterized with abilities to perturb

DEFT

Metabolic Disorders as Consequences of Drug-Induced Energy Deficits,production under pathological conditions, e.g., ketone bodies in hypoglycemia or lactate after cerebral ischemia. Free fatty acids and glycerol are metabolized only in very small amounts (H. and M. 1983).