Plating potential

Peptides in the a-conotoxin family are inhibitors of nicotinic acetylcholine receptors. They were first isolated from C. geographus venom as components which cause paralysis in mice and fish when injected intraperitoneally (27). Early physiological experiments (28) indicated that a-conotoxins GI, GII, and GIA (see Table III) all act at the muscle end plate region. Mini end-plate potentials and end plate potentials evoked in response to nerve stimulation are inhibited in the presence of a-conotoxins in the nM to pM range. a-Conotoxin GI was subsequently shown to compete with rf-tubocurarine and a-bungarotoxin for the acetylcholine receptor (29). 

Sea urchin toxins extracted from spines or pedicellariae have a variety of pharmacological actions, including electrophysiological ones (75). Dialyzable toxins from Diadema caused a dose-dependent increase in the miniature end-plate potential frequency of frog sartorius muscle without influencing membrane potential (76). A toxin from the sea urchin Toxopneustes pUeolus causes a dose-dependent release of histamine (67). Toxic proteins from the same species also cause smooth muscle contracture in guinea pig ileum and uterus, and are cardiotoxic (77). 

Because of differing sensitivities and the natural levels of free metal or the anodic scanning voltammetric labile metal, cadmium, and copper in seawater are analysed using a 10 minute plating time, a -1.0V plating potential, and scanning in 6.67 mV/s increments. Zinc determinations can be made on a fresh aliquot of sample to eliminate any possible effects due to Cu-Zn inter-... 

FIGURE 6-1 Path of excitation in a simplified spinal reflex that mediates withdrawal of the leg from a painful stimulus. In each of the three neurons and in the muscle cell, excitation starts with a localized slow potential and is propagated via an action potential (a.p.). Slow potentials are generator potential (g.p.) at the skin receptor the excitatory postsynaptic potentials (e.p.s.p.) in the interneuron and the motoneuron and end-plate potential (e.p.p.) at the neuromuscular junction. Each neuron makes additional connections to other pathways that are not shown. 

Liley, A. W. The quantal components of the mammalian end-plate potential. /. Physiol. (Lond.) 133 571-587,1956. 

EPP evoked end-plate potential 5-HIAA 5-hydroxyindoleacetic acid... 

HPTLC high-performance thin layer chromatography MEPP miniature end-plate potential... 

Acetylcholine Mescaline, in micromolar concentrations, decreases the release of acetylcholine at the neuromuscular junction, with subsequent effects on end-plate potentials and motor function (Ghansah et al. 1993). Whether or not any similar effect occurs on central cholinergic systems has not been investigated. 

Behavioral and motor effects Mescaline and its analogs inhibit cholinergic neuromuscular transmission by blocking release of acetylcholine and reducing end-plate potentials in the micromolar range (Ghansah et al. 1993). This effect has not been investigated in humans, but it could reduce the force of muscle contractions and motor control. 

Wagley, P.F. 1957. A study of end-plate potentials. Observations on the actions of certain oximes. CWLR 2145. 

Flow does the release of neurotransmitter occur That the release is "quantal," i.e., involving the entire content of a vesicle, was established from the observation of miniature end-plate potentials. These are fluctuations in the postsynaptic potential observed under conditions of weak stimulation of the presynap-tic neuron. They reflect the randon release of neurotransmitter from individual vesicles.553 Normally, a strong impulse will release on the order of 100-200... 

Katz, B. Fatt, P. (1951). An analysis of the end-plate potential recorded with an intracellular electrode. J. Physiol. Lond. 115,320-370. 

Acetylcholine and agents acting at the autonomic ganglia or the neuromuscular junctions interact with nicotinic cholinergic receptors to initiate the end plate potential in muscle or an excitatory postsynaptical potential in nerve. The nicotinic receptor in skeletal muscle is a pentamer composed of four distinct subunits. 

Williamson LC, Neale EA (1998) Syntaxin and 25-kDa synaptosomal-associated protein differential effects of botulinum neurotoxins Cl and A on neuronal survival. J Neurosci Res 52 569-83 Williamson LC, Halpem JL, Montecucco C, Brown JE, Neale EA (1996) Clostridial neurotoxins and substrate proteolysis in intact neurons botulinum neurotoxin C acts on synaptosomal-associated protein of 25 kDa. J Biol Chem 271 7694-9 Wilson HI, Nicholson GM, Tyler MI, Howden ME (1995) Induction of giant miniature end-plate potentials during blockade of neuromuscular transmission by textilotoxin. Naunyn Schmiede-bergs Arch Pharmacol 352 79-87... 

Liu J, Wan Q, Lin X et al (2005) a-Latrotoxin modulates the secretory machinery via receptor-mediated activation of protein kinase C. Traffic 6 756-65 Long SB, Campbell EB, Mackinnon R (2005) Crystal structure of a mammalian voltage-dependent Shaker family K+ channel. Science 309 897-903 Longenecker HE, Hurlbut WP, Mauro A et al (1970) Effects of black widow spider venom on the frog neuromuscular junction. Effects on end-plate potential, miniature end-plate potential and nerve terminal spike. Nature 225 701-3... 

Many plating protocols advocate the use of a flash step where a significantly higher overpotential is applied to ensure that the entire substrate is covered with metal before the potential is reduced to the plating potential. This has been shown to be effective in ionic liquid and significantly improves the corrosion resistance of the coatings [7]. 

In contrast to the large positive accelerating plate potential, the grid is held at a relatively small negative "control" or "grid" potential or bias Ec or Eg... 

Acetylcholine receptors on the motor end plate bind acetylcholine, which opens ligand-gated ion channels. This allows movement of Na into and K out of the myocyte, producing a local depolarisation of the motor end plate (the end-plate potential). 

The technical problems involved with any attempt to use analogously systematic research approaches to a potential transmitter in the central nervous system are great. Peripheral synapses can be isolated by microdissection, they can remain functional in an isolated profusion experimental situation for hours, and their activation can be manifested by clearly defined and measurable phenomena (such as the miniature end-plate potential or the contraction of smooth muscle). The central nervous system has little in the way of focal synaptic regions. The dendrites and the cell bodies of central neurons are densely covered with synapses, many of which may be of a chemically heterogenous nature. In addition, the extra-neuronal space is packed with a tangle of glia, closely approximating the membranous surfaces of nerve cells and possibly intrinsically important to their function. This makes the isolated, chemical manipulation of central synapses extremely difficult. (Mandell and Spooner 1968, p. 1443)... 

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