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PubMed1992

Assessment of the cariogenic potential of fruit fingers, muesli bars and jelly beans.

Intra-oral tests of a fruit bar, a muesli bar and jelly beans were performed to establish their cariogenic potential by means of enamel hardness changes. Little difference was found when the fruit finger and muesli bar were compared. Surprisingly, the jelly beans did not produce a greatly increased degree of softening when compared with the fruit fingers. Statistical significance was not reached in either of the experiments carried out.

Adult↗
PubMed1999

Frequent use of sugar products by schoolchildren in 20 European countries, Israel and Canada in 1993/1994.

The aim of this study was to describe the daily use of certain between-meal sugar products (soft drinks and sweets) of schoolchildren in 20 European countries, Israel and Canada as a part of the Cross-National Survey on Health Behaviour in School-Aged Children--a WHO Collaborative Study. The data were collected using standardised anonymous questionnaires in school classrooms during the 1993/1994 school year. In each country nationally or regionally representative samples of about 1,300 schoolchildren (450 in Greenland) were targeted. Use of sugar products was analysed according to sex, age, country, self-reported school performance and self-reported family economy. One third to one half of the children (30-48 per cent) drank coke or other soft drinks more than once a day in Israel, Northern Ireland, Scotland, the Slovak Republic and Flemish-speaking Belgium. Use of soft drinks was very uncommon in Finland, Sweden, Norway, Denmark, Latvia and Estonia. The strongest association (odds ratios) was between the use of soft drinks and good family economy; in Russia (20.3), in Lithuania (11.3), in Latvia (10.0), in Poland (8.5) and in Estonia (8.0). In Israel, Scotland, Northern Ireland, Russia and French-speaking Belgium 41-29 per cent of the children ate sweets more than once a day. Boys drank soft drinks and ate sweets slightly more often than girls did. In conclusion, large differences were found between the different countries in the frequency of use of soft drinks and sweets. This should be considered when developing the content of oral health promotion programmes.

Achievement↗
PubMed2003

The effect of a 2% zinc citrate, 0.3% Triclosan dentifrice on plaque acid production following consumption of a snackfood.

OBJECTIVES: A) To assess plaque lactate production following consumption of three foods (cake, chocolate/caramel bar, sweetened coffee), and B) To measure the effect of a fluoride dentifrice containing 2% zinc citrate and 0.3% Triclosan on plaque lactate and pH drop following consumption of cake. METHODS: A) 10 subjects completed the first study. Plaque samples taken before and at 8,15 and 30 minutes after eating. Samples were analysed for lactate via Capillary Electrophoresis. B) 30 subjects completed the second study. Plaque samples were taken before and after cake and use of test dentifrice or no treatment control. Plaque pH and lactate content were assessed. RESULTS: A) Plaque lactate levels increased after all three foods; peak lactate levels occurred 8 minutes after eating. B) Plaque lactate concentrations after eating cake were 39.2mM for the control treatment and a significantly lower value, 23.6mM, for the test 2% zinc citrate, 0.3% Triclosan dentifrice. After food challenge, pH values were 5.53 for the no treatment group and a significantly higher value of 5.79 for the test dentifrice group. CONCLUSIONS: A toothpaste containing 2% zinc citrate, 0.3% Triclosan can significantly reduce plaque lactate generation and pH drop induced by cake, compared to no treatment control.

Adolescent↗
PubMed1986

Stimulation by noradrenaline of inositol phospholipid breakdown in the rat hippocampus: effect of the ambient potassium concentration.

The stimulation by noradrenaline (NA) of inositol phospholipid (PI) breakdown has been studied using rat hippocampal miniprisms. Pretreatment with the monoamine oxidase inhibitor, pargyline, potentiated the stimulation produced by NA. On the other hand, pargyline pretreatment did not affect the stimulation of PI breakdown by the alpha 1-adrenoceptor agonist phenylephrine. NA- and phenylephrine-stimulated PI breakdown were enhanced by increasing the ambient potassium concentration in the assay from 5.88 to 18.2 mM. This enhancement did not, in the case of NA, change either the EC50 value for this agonist (2-3 microM) or the pA2 value for the competitive antagonism of the stimulation by the alpha 1-antagonist prazosin (pA2 value 9.2). Time-courses of the NA-stimulated PI turnover in different brain regions indicated that the rate of stimulation was in the order frontal cortex greater than hypothalamus greater than or equal to hippocampus much greater than cerebellum.

Animals↗
PubMed1966

The composition f human saliva secreted in response to a gustatory stimulus and to pilocaprine.

1. The composition of human saliva secreted in response to sour lemon drops (S.L.D.), and pilocarpine, was studied.2. At a given flow rate, pilocarpine-stimulated submandibular and parotid saliva contained less sodium and potassium and an equivalent amount of inorganic phosphate, and parotid saliva also contained more calcium and protein than did the corresponding types of S.L.D.-stimulated saliva.3. Prolonged S.L.D. stimulation did not cause a depletion in the protein concentration of either parotid or submandibular saliva and neither this procedure nor pilocarpine stimulation altered the proportions of the different proteins secreted.4. Pilocarpine was judged to be an inadequate substitute for more physiological, gustatory stimuli.

Calcium↗
PubMed1976

Two types of extrajunctional L-glutamate receptors in locust muscle fibres.

L-glutamate applied iontophoretically to the extrajunctional membrane of locust muscle produced a biphasic response, depolarization followed by hyperpolarization (i.e. DH-response). Applying L-glutamate and DL-ibotenate from multibarrel micropipettes allowed comparison of their extrajunctional responses. While glutamate produced a two component response, ibotenate produced a single component H-response. 2. The equilibrium values for the H-responses to L-glutamate and DL-ibotenate applied at the same extrajunctional site were very similar. The equilibrium value was 59-5 +/- 5-4 mV indicating an increased Cl- conductance. The H-response was reversed and abolished in Cl- free medium. Picrotoxin 10(-3) M selectively blocked the H-component of the DH-response in a reversible manner. 3. The possibility that the D- and H-responses arose from the activation of two distinct types of extrajunctional glutamate receptors was investigated. Desensitization of the glutamate H-response by ibotenate and vice versa indicated the presence of an extrajunctional H-receptor sensitive to glutamate and ibotenate and an extrajunctional D-receptor sensitive to glutamate and insensitive to ibotenate. The junctional depolarizing response to glutamate was insensitive to ibotenate. 4. The presence of junctionally occurring H-receptors could not be discounted, although, if present, they were not measurably activated by the excitatory transmitter. 5. Double logarithmic plots (coulomb dose vs. response) for the actions of glutamate and ibotenate on H-receptors had values of 0-75, indicating that both drugs act on the same receptors with similar mechanisms. The value for the action of glutamate on the D-receptors was 1-5. 6. While the extrajunctional D-receptors show analogies to the extrajunctional ACh receptors in vertebrate muscle, the significance of the extrajunctional H-receptors remains speculative.

Animals↗
PubMed1976

Effects of botulinum toxin on neuromuscular transmission in the rat.

1. Botulinum toxin (BoTx) type A partially blocks spontaneous transmitter release from nerve terminals in the rat. Minature end-plate potentials (m.e.p.p.s) are present at all end-plates, initially with a low frequency but increasing with time after posoning. Their amplitude distribution is at first skew with a predominace of very small m.e.p.p.s but, after a few days, larger than normal m.e.p.p.s appear. 2. Tetanic nerve stimulation, Black Widow Spider Venom, the Caionophore A 23187 or mechanical damage to nerve terminals increases the frequency of m.e.p.p.s and alters the amplitude distribution of m.e.p.p.s towards a normal Gaussian one; the m.e.p.p. size approaches that seen at normal end-plates. This was seen at any time after poisoning. 3. Nerve stimulation gives rise to end-plate potentials (e.p.p.s) of low amplitude and high failure rate. Statistical analysis indicates that evoked release is quantal in nature and follows Poisson statistics, quantum size being initially very small, but after a few days approaching normal size. Short-term tetanic nerve stimulation reversibly increases the quantum content of e.p.p.s and during early stages of paralysis long-term (2 hr) stimulation causes an apparently permanent increase in quantum size. 4. Raising the extracellular Ca concentration from 2 to 16 mM increases the frequency of m.e.p.p.s in normal muscle but not in BoTx poisoned ones. K-free medium or ouabain, which are believed to raise the intracellular Ca concentration in nerve terminals, similarly increases m.e.p.p. frequency in normal but not in poisoned muscles. When the Ca-ionophore A 23187 is used together with high extracellular Ca (greater than 4 mM) massive release of transmitter occurs from poisoned terminals. 5. The extracellular Ca concentration which causes a certain level of transmitter release in reponse to nerve impulses is considerably higher at BoTx poisoned end-plates than at normal ones. The slope value for Ca dependence of transmitter release is about 1-5 compared with about 3 at normal end-plates. 6. Tetraethylammonium (TEA) greatly increases the amount of transmitter released by nerve impulses and restores neuromuscular transmission during all stages of poisoning, although it has not effect on spontaneous transmitter release. In the presence of TEA the power relation between Ca concentration and quantum content at the BoTx poisoned end-plate is similar to that seen at normal end-plates. 7. It is suggested that in BoTx poisoning the mechanism for transmitter release has a reduced sensitivity to Ca, and the level for activation by intracellular Ca is elevated. Once the intracellular concentration of Ca is raised to this level, by tetanic nerve stimulation, mechanical injury to nerve terminals, the Ca-ionophore or the prolongation of the nerve action potential with TEA, augmented transmitter release occurs, similar to that which occurs in normal nerve terminals at a lower level of Ca.

Animals↗
PubMed1978

Glutamate sensitivity and distribution of receptors along normal and denervated locust muscle fibres.

1. Factors influencing the glutamate sensitivity of extrajunctional regions of innervated and denervated locust muscle fibres have been investigated. Properties of the two types of extrajunctional glutamate receptors, D- and H-receptors, have been studied in regions of high and low sensitivity. 2. The low level of extrajunctional sensitivity which is normally present in innervated fibres was 20-30 times higher at the muscle-tendon junction than at other sites; increased sensitivity extended about 20-40 micron from the tendon. After denervation or localized damage the entire extrajunctional sensitivity was increased approximately 100 times above control levels. 3. Applying L-glutamate (which activates D- and H-receptors) and DL-ibotenate (which activates H-receptors) from multibarrelled micropipettes showed that increased extrajunctional sensitivity resulted from an increase in D-receptors while H-receptors were apparently unchanged. 4. Coulomb dose vs. response relationships for the action of glutamate on D-receptors were similar when obtained at the muscle-tendon junction and nerve-muscle junction of innervated fibres or at extrajunctional regions in denervated fibres. 5. Time course of onset and percentage desensitization of D- and H-receptors in innervated fibres were similar. The percentage desensitization of D-receptors in extrajunctional regions of high sensitivity was greatly reduced. 6. It is suggested that D- and H-receptors are independent and that the trigger for increased receptor sensitivity acts specifically on D-receptors. In all respects so far studied, the D-receptors resemble extrajunctional ACh-receptors in vertebrate muscle.

Animals↗
PubMed1978

Glutamate current noise: post-synaptic channel kinetics investigated under voltage clamp.

1. Analysis of voltage-clamped noise has been used to investigate the operation of glutamate receptors and associated channels at the locust nerve-muscle junction. Channels opened by glutamate and an agonist have been compared. 2. Glutamate-induced current fluctuations have a power spectrum with a single (1/frequency2) component which fits a simple model for the operation of channels. The form of the spectra for glutamate voltage noise and for 'background' noise has been determined. 3. The single channel conductance was estimated from the spectra, gamma glutamate = 122 +/- 0.4 (S.E.) pS. This estimate is independent of membrane potential and of the amplitude of membrane current change produced by glutamate. 4. The rate constant, alpha, for the closing of glutamate-operated channels depends exponentially on membrane potential, conforming to the equation alpha = approximately alphaeetaVm (approximately alpha = 0.26 +/- 0.014 msec-1, eta = 0.0054 +/- 0.001 msec-1); the duration of the channel lifetime (tau) decreases with hyperpolarization. Membrane potential dependence of alpha reduces as temperature is lowered. 5. For glutamate-operated channels, the temperature dependence of alpha and gamma fits the Arrhenius equation; alpha and gamma decrease exponentially as a function of T-1 (degrees K) with a descrete change in slope at about 6 degrees C, indicating a change in the activaiton energies of the respective rate processes. 6. Spectra of quisqualate-induced current fluctuations have the same form as spectra for glutamate noise. The single channel conductance was estimated from the spectra, gamma quisqualate = 120 +/- 3.9 (S.E.) pS. 7. The rate constnt, alpha, for the closing of quisqualate-induced channels depends exponentially on membrane potential. The duration of the open state for quisqualate channels was 2.2 times longer than for glutamate channels. 8. For glutamate receptors the voltage-sensitivity of the channel life-time is in the opposite direction to that of ACh receptors in vertebrate muscle. Possible explanations for the sharp change in the activation energy of the rate processes associated with the channel are discussed.

Alanine↗
PubMed1979

End-plate currents and acetylcholine noise at normal and myasthenic human end-plates.

1. The amplitudes and time courses of miniature end-plate currents (m.e.p.c.s) have been compared at normal and myasthenic (MG) human end-plates studied under voltage clamp. The m.e.p.c. amplitude at MG end-plates is reduced to about one third normal; mean m.e.p.c. (normal) = 2.6 +/- 0.2 nA, mean m.e.p.c. (MG) = 1.0 +/- 0.1 nA. The decay time constant of m.e.p.c.s (tau m.e.p.c.) is very similar at normal and MG end-plates; tau m.e.p.c. (normal) = 1.70 +/- 0.1 msec, tau m.e.p.c. (MG) = 1.80 +/- 0.13 msec (Vm = - 80 mV. T = 23 degrees C). 2. The equilibrium potential of the end-plate current (e.p.c.) at normal and myasthenic human end-plates is close to 0 mV. 3. Decay time constants tau e.p.c. and tau m.e.p.c. increase exponentially with membrane hyperpolarization. The voltage sensitivity of the time constants was similar at normal and MG end-plates. 4. Both normal and myasthenic e.p.c.s are greatly prolonged in the presence of neostigmine (10(-6) g/ml.). At the same time the voltage sensitivity of tau e.p.c. is slightly reduced. 5. In response to steady ionophoretically applied ACh the mean membrane currents obtained at MG end-plates were smaller than the normal under similar conditions. 6. Analysis of end-plate current noise obtained during the steady application of acetylcholine (ACh) to voltage clamped normal and MG human end-plates showed that the amplitude of the elementary current event (gamma) and the average channel life-fime (tau noise) was similar at the two sites: tau noise (normal) - 1.54 +/- 0.04 msec, tau noise (MG) = 1.60 +/- 0.11 msec; gamma(normal) - 22.3 +/- 1.57 PS, gamma (MG) = 20.25 +/- 1.93 pS (Vm = - 80 mV, T = 23 degrees C). The voltage sensitivity of the channel life time, measured from end-plate current noise, was similar at normal and MG end-plates. 7. At normal human end-plates a packet of transmitter opens about 1500 channels whereas at MG end-plates a packet opens only about 600 channels. It is calculated that the size of the transmitter packets released from MG-terminals is at least as large as the packet of the ACh released from normal human nerve terminals.

Acetylcholine↗
PubMed1980

Induction of action potentials in cultured slow muscle fibres of the frog.

1. Slow muscle fibres of the frog were maintained in a simple organ culture system for up to 28 days at 18 degrees C. Slow fibres cultured for one week resembled innervated fibres in their lack of ability to generate an action potential. 2. By 10 days a few fibres had acquired the action potential mechanism and in muscles cultured for 28 days all slow fibres examined were capable of generating action potentials most of which reached or exceeded 0 mV membrane potential. 3. Slow muscle fibres which were denervated for two weeks in vivo retained their ability to generate overshooting action potentials after 4 weeks of culture. Thus, in the culture system described, slow muscle fibres are capable of developing action potentials and the action potential mechanism in these fibres remains for at least one month in culture.

Action Potentials↗
PubMed1980

On the release of transmitter at normal, myasthenia gravis and myasthenic syndrome affected human end-plates.

1. Transmitter release has been studied at normal, myasthenia gravis (m.g.) and myasthenic syndrome (m.s.) affected human end-plates. At normal and diseased end-plates evoked transmitter release is Poisson for a mean quantal content, m less than ten. 2. The relation between log m and log [Ca]o, at normal and m.g. end-plates is linear, with a slope of 3.3-3.4. The value of m at m.g. end-plates is about five times larger than normal, below Ca 0.7 mM (Mg, 2mM). This difference in m is reduced at higher Ca levels. 3. The slope of the relation between log m.e.p.p. frequency and log [K]o is similar at normal and m.g. end-plates. Over its linear portion the relationship has a slope of approximately 6. 4. Fluctuations in the latency of evoked transmitter release were compared at normal and m.g. nerve terminals. At normal end-plates the probability of release reaches a peak about 0.3-0.4 msec after unitary e.p.p.s of the shortest latency and returns to zero about 1.0 msec after the peak. At m.g. end-plates the distribution of latencies shows less uniformity. 5. At m.s. end-plates m is approximately 5 in normal Ringer solution (2 mM-Ca, 1 mM-Mg). The relation between log m and log [Ca]o is linear, with a slope of 1.0-1.5. The K dependence of m.e.p.p. frequency appears reduced at m.s. end-plates. 6. Assuming a co-operative mechanism for transmitter release at normal human motor nerve terminals, the dissociation constant for the Ca complex is about 1.6X10(-3) M and the dissociation constant for the Mg complex is about 1.0X10(-3) M. 7. It is concluded that the presynaptic changes, at m.g. end-plates, are not the primary cause of the defect in nerve muscle transmission. At m.s. end-plates the presynaptic changes are sufficient to account for failure in transmission. Possible mechanisms for the abnormalities in transmitter release are considered.

Action Potentials↗
PubMed1981

Properties of end-plate channels in rats immunized against acetylcholine receptors.

1. Rats injected with purified acetylcholine receptors (AChR) extracted from electric organs of Torpedo marmorata showed clinical symptoms consistent with the development of experimental myasthenia gravis.2. Sera of rats with this disease contain high levels of anti-AChR antibodies. However, no simple correlation was found between antibody titre and miniature end-plate current (m.e.p.c.) amplitude.3. M.e.p.c.s. at the end-plates of rats injected with AChR (Anti-R), emulsified in complete Freund Adjuvant (CFA), were reduced to about one third the size of controls taken from rats injected only with CFA (Anti-CFA). Mean m.e.p.c. (Anti-R) = 0.73 +/- 0.06 nA; mean m.e.p.c. (Anti-CFA) = 2.43 +/- 0.12 nA (V(m) = -80 mV, T = 20 degrees C).4. The m.e.p.c. decay time constant, tau(m.e.p.c.), is similar at immunized and control rat end-plates. tau(m.e.p.c.) (Anti-R) = 1.32 +/- 0.06 msec; tau(m.e.p.c.) (Anti-CFA) = 1.31 +/- 0.06 msec (V(m) = -80 mV, T = 20 degrees C).5. The end-plate current decay time constant, tau(e.p.c.), is similar at immunized and control end-plates and in both cases depends exponentially on membrane potential. The change in membrane potential required to produce an e-fold change in tau(e.p.c.) is 102.0 +/- 5.72 mV at immunized (Anti-R) end-plates and 92.3 +/- 6.14 mV at control (Anti-CFA) end-plates at T = 10 degrees C.6. Acetylcholine noise was examined at immunized and control rat end-plates at 10 degrees C. Analysis of noise indicates that the single channel conductance, gamma, and mean channel life-time, tau(noise), are essentially unchanged by immunization against AChR. gamma (Anti-R) = 13.15 +/- 0.53 pS; gamma (Anti-CFA) = 12.50 +/- 0.50 pS; tau(noise) (Anti-R) = 2.9 +/- 0.18 msec; tau(noise) (Anti-CFA) = 2.68 +/- 0.14 msec (V(m) = -80 mV, T = 10 degrees C).7. Mean quantal content and Ca(2+) dependence of the end-plate potential are unchanged at immunized end-plates.8. It is concluded that at immunized end-plates the number of activated receptor-channel complexes is reduced without modification of single channel properties. In this respect the immunized rat end-plate is a good model for myasthenia gravis affected human end-plates.

Acetylcholine↗