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Neuromuscular system biology

The biological targets of paralytic conotoxins are presumably ion channels and receptors in the fish neuromuscular system. Amphibian, avian, and mammalian systems may also be affected by a -, a-, and x-conotoxins. However, specific conotoxins vary in their phylogenetic spectrum and detailed physiological effects in vivo. [Pg.267]

Biological functions of the structure. The trematode tegument is structurally adapted for transport, immune evasion and communication with the neuromuscular system (via gap junctions). Numerous pits at the surface of the tegument markedly increase the surface area of the parasite, which is consistent with a transport function (see below). The fact that all of the pits in schistosomes examined in situ contain erythrocytes (55) suggests that these structures are open to the external environment. The tegument is less pitted in F. hepatica, but numerous invaginations of the surface effectively increase the surface area. [Pg.212]

The ability of a parasite to move to different sites in its host and to maintain its position in host body fluids, where appropriate, is crucial to the parasite s survival. Understanding the mechanisms underlying its motile capabilities, particularly at the level of its neuromuscular system, is of great importance both for an understanding of basic parasite behavior and biology and for the development of anthelmintic compounds. This chapter will focus on the chemical signals affecting the neuromuscular systems of adult parasitic helminths with emphasis on putative transmitters and modulators in the trematodes, cestodes and nematodes. [Pg.258]

Synthetic AFl and AF2 have potent biological activity on the neuromuscular system of A. suum. Injection of AFl or AF2 produced a local paralysis near the injection site. In a muscle strip preparation, both AFl and AF2 produced multiple effects on muscle tension, including relaxation, contraction, and induction of rhythmic activity (196,197). Intracellular recording techniques show that AFl, at 10 -10 m, short-circuits electrical activity in inhibitory, but not excitatory motoneurons by opening channels in their membranes (194). The input resistance of these cells is drastically reduced by AFl this effect is due, at least in large part, to the presence of receptors for AFl on the inhibitory motoneuron since, when synaptic transmission is blocked with Co, the... [Pg.275]

Enzyme Inhibition. Some materials produce toxic effects by inhibition of biologically vital enzyme systems, leading to an impairment of normal biochemical pathways. The toxic organophosphates, for example, inhibit the cholinesterase group of enzymes. An important factor in thek acute toxicity is the inhibition of acetylocholinesterase at neuromuscular junctions, resulting in an accumulation of the neurotransmitter material acetylcholine and causing muscle paralysis (29) (see Neuroregulators). [Pg.228]

Koopowitz, H. (1973). Organization of primitive nervous system. Neuromuscular physiology of Gyrocotyle urna, a parasitic flatworm. Biological Bulletin, 144 489-502. [Pg.330]

Milic-EmUi, J. and Zin, W.A. 1986. Relationship between neuromuscular respiratory drive and ventilatory output. In P.T. Macklem and J. Mead (Eds.), Handbook of Physiology, sec 3, The Respiratory System, Vol. 3, Mechanics of Breathing, part 2, pp. 631-646, Washington, DC, American Physiological Society. Milsum, J.H. 1966. Biological Control Systems Analysis. New York, McGraw-Hill. [Pg.408]


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