Miniature end-plate potentials

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). 

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

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... 

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... 

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)... 

Laskowskl, M.B., Olson, W.H. and Dettbarn, W.D., 1976 Motor end-plate degeneration coincident with cholinesterase (Ch ) Inhibition and Increased miniature end-plate potential frequency. (Abstract) Fed. Proceed. 35 800. 

Second, divalent Pb is similar in many aspects to Ca and may exert a competitive action in body processes such as mitochondrial respiration and neurological functions. Lead can compete with Ca for entry at the presynaptic receptor. Since Ca evokes the release of acetylcholine across the synapse, this inhibition manifests itself in the form of decreased end plate potential. The miniature end plate potential release of subthreshold levels of acetylcholine has been shown to be increased (Barton et al. 1978). The close chemical similarity between Pb and Ca may partially account for the fact that they seem interchangeable in biological systems and that 90% or more of the total body burden of Pb is found in the skeleton. 

Berberine was observed to reduce the amplitude of spontaneous miniature end plate potentials in the frog neuromuscular junction. At low concentrations, berberine diminished the frequency of miniature potentials, but increased it when the concentration exceeded a certain value [250]. 

Brooks, V.B. 1956. An intracellular study of the action of repetitive nerve volleys and of botulinum toxin on miniature end-plate potentials. J. Physiol. (Land.) 134 264—277. 

Polyneuronal innervation is lost during the first 2 weeks of life (Brown et al., 1976 O Brien et al., 1978). There is a 100-fold increase in miniature end-plate potentials between the first and second postnatal week of life (Diamond and Miledi, 1962 Nakajima et al., 1980). This coincides very closely with the postnatal decline in IGF-II gene expression. It is postulated that the increased neuromuscular activity (miniature end-plate potentials), through heightened feedback inhibition, causes down-regulation of IGF-II gene expression. The decline in IGF-II activity results in an environment that can no longer support multiple synapses and polyneuronal innervation is lost. 

Nonelectrogenic functions. During the resting state, there is a continual slow release of isolated quanta of the transmitter that produces electrical responses at the postjunctional membrane [miniature end-plate potentials (mepps)] that are associated with the maintenance of physiological responsiveness of the effector organ. A low level of spontaneous activity within the motor units of skeletal muscle is particularly important because skeletal muscle lacks inherent tone. The activity and turnover of enzymes involved in the synthesis and inactivation of neurotransmitters, the density of presynaptic and postsynaptic receptors, and other characteristics of synapses probably are controlled by trophic actions of neurotransmitters or other trophic factors released by the neuron or the target cells. 

It is not clear whether the biological effects of the toxin are all sequelae of its effects on membranes. The toxin provokes an increase in miniature end-plate potential frequency at the neuromuscular junction, leading eventually to a depletion of presynaptic vesicles [32]. Increased calcium influx as a result of toxin action on the nerve terminal may be a prime event, but it is difficult to understand the specificity of action of the toxin in the biological situation. 

Cesium exhibits marked effects on the nervous system, both peripherally and centrally. This may be the consequence of the purported interchangeability of cesium with other group I metals. Certainly cesium ions will increase the frequency of miniature end-plate potentials, thought to be due to the slow entry of cesium ions into the nerve terminal [32]. In the central nervous system, it seems that cesium can share the same receptor as glycine and exerts its effects by activating the same chloride channel as the inhibitory neurotransmitter, glycine [33]. Indeed, in consequence of this action, cesium has been implicated as a causative agent of some epileptiform seizures [34]. More recently, pretreatment of rats with cesium chloride, followed by administration of the monoamine oxidase inhibitor tranylcypramine, has been shown to enhance 5-hydroxytryptamine (5-HT) behavioral syndrome. This may be due to either an increased amount of 5-HT synthesis and/or release, or a direct enhancement of the postsynaptic action of 5-HT [34b]. 

Lead is also known to increase miniature end-plate potential frequency at the unstimulated neuromusculeir junction, indicating that Pb causes an increase in spontcmeous trcmsmitter release. These results, in contrast to the blocking effect of Pb on transmitter-stimulated release, suggest that there may be two mechanisms, one for stimulated and one for spontemeous trems-mitter release. 

Neuromuscular synapses. Lanthanum can act as a surrogate for Ca in transmitter release at (mouse) motor nerve terminals, and cause an increased frequency of miniature end-plate potentials at the neuromuscular junction (Curtis, Quastel et al. 1986). According to Provan and Miyamoto (Provan and Miyamoto 1992) lanthanum enters the terminal through Na channels and promotes Ca release from intracellular organelles. 

To confirm the prejunctional action of the enterotoxin, end-plate potentials before and after the treatment of the diaphragm preparation with the enterotoxin. The resting membrane potentials of the muscle fibers were not affected by the enterotoxin measurement. However, the enterotoxin reduced frequency, but not mean amplitude or amplitude distribution, of miniature end-plate potentials (Table 1). The results indicate that the release of transmitter was inhibited by the treatment with the enterotoxin, but that the response of acetylcholine-receptor in the postjunctional membrane to the transmitter was unaffected. 

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