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Biomedical subjects

W Finger

Publications and source records attributed to W Finger.

At least 19 recordsLinked to original sources
PubMed1995

NMDA-induced whole-cell currents and single channel conductances in tectal neurons during two stages of early development of chicken.

In cultured tectal neurons of embryonic chicken N-methyl-D-aspartate (NMDA) receptor currents were investigated during two stages of development. Stage I tectal cells were cultivated for 1-5 days from embryonic day 6 or 7, and stage II tectal cells for 10-30 days. Steady state inward currents induced by NMDA were usually several times smaller in tectal cells of stage I than in tectal cells of stage II. At the somata of stage I tectal cells, NMDA-activated single channels with a mean conductance of about 55 pS could be recorded. In tectal cells of stage II, however, NMDA receptor channels were predominantly observed at cellular processes and a mean single channel conductance of about 72 pS was found. Our results suggest changes in regional distribution and function of NMDA receptors during early embryogenesis in the chicken tectum.

Animals↗
PubMed1993

A 5-year report on a enamel-dentinal bonding agent and microfilled resin system.

The aim of this study was to examine the clinical performance of the Gluma enamel dentinal bonding system and Pekalux microfilled composite resin. Sixty esthetic restorations were placed by three different operators. After 5 years of clinical performance, 40 restorations were evaluated. Alpha scores were given to 25 restorations for marginal integrity, 21 for color stability, and 27 for anatomic form. Bravo scores were given to 11 restorations for marginal integrity, 13 for color stability, and 10 for anatomic form. Six restorations had to be replaced. The results of this study reveal the importance of the periodic maintenance of restorations; every patient was reexamined, underwent conservative restoration polishing, and attended an oral hygiene session every 6 months.

Adolescent↗
PubMed1992

Influence of buffered and unbuffered acetylsalicylic acid on dental enamel and dentine in human teeth: an in vitro pilot study.

An in vitro study was conducted to investigate the erosive effect of buffered and unbuffered acetylsalicylic acid (ASA) on dental enamel and dentine in human teeth by scanning electron microscopy. In order to standardize the specimens and to improve comparability the dental enamel and dentine were superficially abraded. The enamel and dentine specimens were therefore particularly sensitive to the influences of acid agents. Concentrated solution of buffered chewable ASA tablets (500 mg ASA and 300 mg calcium carbonate in 5 ml water) showed no changes in the enamel surface structure after exposure times of 1 min, 5 min and 60 min. In contrast, minimal corrosive effects were already seen after exposure of the enamel surface to the unbuffered ASA solutions for 1 min. After exposure times of 5 min and 60 min erosion of the enamel was more pronounced. Immersion in the unbuffered ASA solution led to clearly visible micromorphological changes on the dentine surfaces even after exposure for 1 min. Exposure of the dentine specimens to the buffered ASA solutions led to only very slight changes in the surface morphology. Therefore, the scanning electron micrograph after exposure to buffered ASA is comparable to the picture of untreated dentine.

Aspirin↗
PubMed1990

Quantal secretion and loss of vesicles induced by veratridine at the crayfish neuromuscular junction.

Experiments were conducted in nerve-muscle preparations of small young crayfish (Austropotamobius torrentium, Astacus astacus). Application of veratridine in the superfusate induced strong quantal release of transmitter. After about 5 min when quantal release had declined to a low level preparations were fixed for electron microscopy. Unlike control preparations, veratridine-treated preparations revealed nerve terminals which were largely depleted of their synaptic vesicles. Our findings suggest that in the presence of veratridine the decline of quantal secretion results from the loss of vesicles caused by tonic nerve terminal depolarization. Moreover, our results indicate that during or after excessive quantal release triggered by veratridine synaptic vesicles may fuse with both the presynaptic membrane and each other.

Animals↗
PubMed1989

Presynaptic effect of gamma-aminobutyric acid on the inhibitory nerve and nerve terminals in the crayfish neuromuscular junction.

Experiments were carried out in voltage-clamped fibres of the opener muscle of the first walking leg or claw of small crayfish. Repetitive discharges in the inhibitory nerve innervating the muscle were induced by adding serotonin (10(-6) mol/l) and forskolin (10(-4) mol/l) to the superfusate. Rates of nerve discharge were determined by recording nerve evoked inhibitory postsynaptic currents (IPSCs) in the voltage-clamped muscle fibre. Subsequently, the effect of gamma-aminobutyric acid (GABA) on the rate of IPSCs in normal and Cl- -deficient superfusate was investigated. In normal superfusate GABA (10(-5) mol/l) abolished the IPSCs whereas in Cl- -deficient superfusate GABA (10(-4) mol/l) enhanced the rate of IPSCs. Moreover, in Cl- -deficient superfusate the rate of asynchronous quantal release of inhibitory transmitter could be enhanced by GABA. The results indicate that in the crayfish neuromuscular junction the inhibitory axon is supplied with GABA receptors which may affect (a) axonal excitation and (b) quantal output at the inhibitory axon terminals.

Action Potentials↗
PubMed1989

Quantal stores of excitatory transmitter in nerve-muscle synapses of crayfish evaluated from high-frequency asynchronous quantal release induced by veratridine or high concentrations of potassium.

At single voltage-clamped opener muscle fibres of crayfish claw, 10-100 mumol/l veratridine increased within a few seconds the rate of asynchronous quantal release, ñ, of excitatory transmitter from ñ less than 1 quantum/s to ñ congruent to 10,000 quanta/s. Thereafter ñ declined exponentially either with a single, tau(2) congruent to 50 s, or with two time constants tau(1) congruent to 19 s, tau(2) congruent to 50 s. In total (t----infinity), about 0.3 million quanta were released by veratridine in a single short fibre of about 1 mm length. These values were estimated by means of the noise analysis technique and they agreed with equivalent parameters of release when 100 mmol/l K+ were used as release stimulus. Strong quantal release could be elicited only once in a single muscle by veratridine. Furthermore, the effect of veratridine on quantal release could be completely prevented by pretreatment with tetrodotoxin. In another nerve-muscle preparation of crayfish, the abdominal superficial extensor muscle, up to 3 million excitatory quanta could be released by veratridine in a single fibre. In the latter muscle veratridine-induced asynchronous quantal release was strongly dependent on the extracellular concentration of Ca2+ whereas in the claw opener dependence of quantal release on extracellular Ca2+ was negligible.

Animals↗
PubMed1989

Mechanical properties and filler fraction of dental composites.

Several mechanical properties of experimental composites and an unfilled resin were studied. The dynamic Young's modulus was measured with a non-destructive dynamic method. The Young's modulus and also the transverse strength were determined statically by means of three-point bending. The hardness was studied by means of Wallace indentation depth measurements, and in vitro wear resistance was assessed under stress-bearing conditions. An exponential regression of the results measured for each property as a function of the volumetric filler fraction was appraised. An excellent correlation was found with each property. This exponential mixture rule is proposed for the study of the mechanical properties of isotropic dental composites.

Composite Resins↗
PubMed1988

Prolonged time course of glutamate-operated single channel currents in neuromuscular preparations of small crayfish and a membrane current triggered by glutamate channel gating.

Single channel currents activated by glutamate were recorded by means of the patch-clamp technique in the abdominal superficial extensor muscle and the claw opener muscle of small (1-3 months old) and large (greater than 16 months old) crayfish. It was found that in small crayfish the time course of glutamate-operated single channel currents was prolonged by a factor of about 4 in these two preparations. In the abdominal superficial extensor muscle, single channel currents activated by 5 mmol/l glutamate had a mean burst length of tau = 2-3 ms in large crayfish and a mean burst length of tau = 8-9 ms in small crayfish. In the claw opener, for large crayfish tau congruent to 0.5 ms and for small crayfish tau = 1.5-2.5 ms resulted (500 mumol/l glutamate). Moreover, single channel currents with long time courses often slowly increased their amplitudes during the open time of the channel and current amplitudes did not decline completely to the baseline after channel closing. In addition, single channel currents with relatively constant amplitude were often followed by a small increasing and decreasing membrane current. The latter results suggest that glutamate channel gating might trigger a membrane current.

Animals↗
PubMed1988

Quisqualate-activated single channel currents in neuromuscular preparations of small and large crayfish.

Single channel currents elicited by 1-5 mumol/l quisqualate in neuromuscular preparations in large (greater than 16 month old) and small (1-3 month old) crayfish were recorded by means of the patch-clamp technique. In preparations from large crayfish single channel currents of variable amplitude (-1 to -12 pA) were induced by quisqualate. The mean burst lengths of these currents were tau approximately equal to 1-2 ms. In the opener muscle of the first walking leg and the contractor epimeralis muscle of small crayfish the mean burst lengths of single channel currents evoked by quisqualate were prolonged by a factor of about 4 (tau approximately equal to 5 ms). Moreover, in the opener muscle of the first walking leg of small crayfish single channel currents of small amplitude (-0.5 to -2.5 pA) were preferentially evoked by quisqualate. By contrast, in the contractor epimeralis muscle of small crayfish mainly single channel currents of large amplitude (-10 to -12 pA) were elicited by quisqualate. The results suggest that at the stage of neuromuscular development characterizing the small crayfish, gating properties of excitatory postsynaptic channels are different from those in adult crayfish. Furthermore, the results obtained in the opener muscle of the first walking leg of small crayfish are consistent with those obtained previously by means of the noise analysis technique.

Animals↗
PubMed1988

Veratridine-induced high-frequency asynchronous release of inhibitory transmitter quanta in crayfish nerve-muscle synapses superfused with normal and low-calcium saline.

Crayfish fibres of opener muscles were voltage clamped to E = -80 mV membrane potential (T = 19-22 degrees C), and veratridine (10-100 mumol/l) was added to the superfusate. Within 30-60 s this caused large fluctuations of the clamp current due to vigorous asynchronous quantal release from the inhibitory nerve terminals along the muscle fibre. Excitatory postsynaptic receptors were previously desensitized by application of 5 mmol/l glutamate. Current fluctuations were evaluated by means of the noise analysis technique. Typically, 100 mumol/l veratridine increased instantaneously the quantal release rate n from n less than 1 quantum/s to n congruent to 10,000 quanta/s. Thereafter, n declined exponentially with a time constant of congruent to 70 s. On average, about 500,000 inhibitory quanta could be liberated in this way from the terminals on a single muscle fibre of congruent to 1 mm length. Serotonin (1 mumol/l) facilitated the effect of lower veratridine concentrations (1-10 mumol/l). In opener muscles veratridine-induced asynchronous quantal release showed little dependence on the bath concentration of Ca2+. The opposite was found for fibres of the superficial abdominal extensor muscle. Beside postsynaptic current fluctuations, veratridine elicited slowly changing average postsynaptic DC-currents which could be explained partly by superposition of individual inhibitory quantal currents. These DC-currents suggest that beside inhibitory quantal release another factor activates inhibitory postsynaptic receptors after application of veratridine.

Animals↗
PubMed1988

Effect of lithium on veratridine-induced quantal and non-quantal release from inhibitory nerve terminals in crayfish muscle.

Muscle fibres of small crayfish were voltage clamped and superfused for about 10 min with Li+ saline (Na+ replaced by Li+) which contained 5 mmol/l glutamate to desensitize excitatory postsynaptic receptors. Then 100 mumol/l veratridine were added to the superfusate which caused strong asynchronous quantal release of inhibitory transmitter. However, in the presence of Li+ strong inhibitory quantal release was only transient. It could be activated a second time by removal of Li+ and readministration of Na+. From the total of 0.7 to 1.1 million quanta released by veratridine only about 30-35% could be released in Li+ saline. The voltage clamp DC-currents recorded during veratridine-induced quantal release suggested that a non-quantal release component is additionally involved. This non-quantal release component was most prominent during the period of quantal release in Li+ superfusate while it was less obvious during the second enhancement of quantal release in normal saline. Together with previous results (Martin and Finger 1988) it may be concluded that quantal release, but not non-quantal release, is decreased by Li+ in the nerve terminals.

Animals↗
PubMed1987

Inhibitory effect of intraterminal lithium on asynchronous release of excitatory quanta induced by veratridine in nerve-muscle synapses of crayfish.

Crayfish muscle fibres were voltage-clamped at E = -80 mV membrane potential and superfused for about 10 min with Li+ saline (Na+ replaced by Li+) which contained picrotoxin to block inhibitory post-synaptic currents. Addition of veratridine (100 mumol/l) caused intense fluctuations in the voltage clamp current within 20-60 s due to vigorous asynchronous quantal release of excitatory transmitter from the nerve terminals distributed over the muscle fibre surface. Most likely, this quantal release resulted from loading the nerve terminals with Li+ via voltage-gated Na+ channels activated by veratridine. However, in the presence of Li+ quantal release was only transient; the quantal release rate, ñ, attained a maximum of congruent to 10,000 quanta/s and then declined exponentially with tau congruent to 10 to 20 s. Removal of Li+ and reapplication of normal Na+ increased ñ a second time. The amount of quanta released in the presence of Na+ was about an order of magnitude larger than that released previously in the presence of Li+. In preparations pretreated with Li+ superfusate for t greater than 45 min no marked quantal release could be elicited by veratridine. The experiments suggest an inhibitory effect of intraterminal Li+ on the quantal release process.

Animals↗
PubMed1987

Single channel currents of different amplitude activated by glutamate in a tonic (slow) crayfish muscle.

Single channel currents were recorded by means of the patch-clamp technique from a tonic (slow) crayfish muscle in the presence of 5 mM glutamate. The experiments were carried out with 'Gigaohm-seals' in the 'cell-attached' mode at 15-17 degrees C. Five classes of single channel currents with different mean amplitudes were resolved: i1 = -0.75 +/- 0.43 (S.D.) pA, i2 = -1.4 +/- 0.4 pA, i3 = -3.5 +/- 0.63 pA, i4 = -8.5 +/- 0.92 pA and i5 approximately equal to 2 X i4, i2, i3 and i4 were recorded at resting membrane potential, Eo approximately equal to -80 mV (pipette potential Vp = 0), while i1 and i5 were recorded at 40 mV hyperpolarized to Eo (Vp = +40 mV). The current most frequently seen was i4 which is the excitatory glutamate-activated single channel current recorded previously by Franke et al. The membrane reversal potentials and channel conductances for i2 and i4 were estimated to be +60 mV (Eo + 140 mV), 13 pS for i2 and +40 mV (Eo + 120 mV), 80 pS for i4. It was assumed that up to 40 i1 currents could superpose in a single patch to generate a DC current of up to -30 pA with current fluctuations the intensity of which increased with the DC current amplitude. Often variable combinations of i1 to i4 currents could be recorded simultaneously in a single patch. In particular, simultaneous activity of i1, i4; i2, i4 and i3, i4 currents was observed in different single patches.

Animals↗
PubMed1987

Differential effect of intraterminal sodium on spontaneous quantal release of transmitter in two neuromuscular junctions of crayfish.

Nerve terminals on the superficial abdominal extensor muscle and the claw opener muscle of small crayfish were loaded with sodium by bath application of 100 mumol/l veratridine in superfusates where normal Ca2+ was removed (low-Ca2+ superfusate). In both preparations this caused an increase in spontaneous quantal release of excitatory and inhibitory transmitter which was evaluated by means of the noise analysis technique. About 2.5 min after application of veratridine, when spontaneous quantal release had largely ceased, the normal Ca2+ concentration was reestablished. This increased transiently the quantal release rate a second time. However, release activated by Ca2+ application was much more vigorous at the superficial abdominal extensor muscle than at the claw opener. At the superficial abdominal extensor muscle on average about 8% of the total number of quanta could be released in low Ca2+ and 92% in normal Ca2+ superfusate, while at the claw opener 75% of the quanta were released in low Ca2+ and 25% in normal Ca2+ superfusate. The experiments suggest that intraterminal sodium has a differential effect in the terminals of the two preparations. Possibly, the intraterminal source from which Na+ may liberate Ca2+ is more restricted in the superficial abdominal extensor muscle than in the opener muscle of the claw.

Animals↗
PubMed1986

Repetitive axonal discharges elicited by serotonin and intracellular adenosine 3',5'-cyclic monophosphate in the crayfish neuromuscular junction.

Experiments were carried out in the opener muscle of the claw of small crayfish. After pretreatment of the preparation with serotonin (5-HT), application of the membrane permeant analogue of adenosine 3',5'-cyclic monophosphate (cAMP), 8-bromoadenosine 3',5'-monophosphate was capable of evoking reversibly repetitive discharges in the inhibitory and excitatory axon. Reducing phosphodiesterase activity with application of either 3-isobutyl-1-methylxanthine or theophylline also elicited repetitive axonal discharges after 5-HT treatment. Moreover, application of forskolin dissolved in ethanol caused repetitive axonal discharges. The chemically induced presynaptic action potentials were detected mainly by their postsynaptic effects, i.e. by recording inhibitory and excitatory postsynaptic currents in voltage-clamped muscle fibres. In addition, nerve spikes were recorded extracellularly. It is concluded that 5-HT and intraaxonal cAMP alter membrane properties of the efferent axons innervating crayfish muscle.

1-Methyl-3-isobutylxanthine↗