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Biomedical subjects

W Finger

Publications and source records attributed to W Finger.

At least 37 records · Page 2Linked to original sources

Spontaneous excitatory postsynaptic currents in crayfish neuromuscular junctions in the absence and presence of serotonin and 3,4-diaminopyridine.

Spontaneous excitatory postsynaptic currents (sEPSCs) were recorded under voltage clamp in short fibres (l less than or equal to 0.6 mm) from opener muscles and the contractor epimeralis muscle of small crayfish. From the amplitude distributions of sEPSCs which could be approximated by a Gaussian function, a mean amplitude ã = -1.16 nA +/- 0.28 (SE) was found for sEPSCs in 16 fibres of the claw opener voltage clamped to E = -60 mV (19-22 degrees C). In the opener of the first walking leg and in the contractor epimeralis muscle ã = -1.1 nA +/- 0.21 (SE; n = 6, -100 mV less than or equal to E less than or equal to -60 mV, 5-10 degrees C) and ã = -2.0 nA +/- 0.2 (SE; n = 4, E = -60 mV, 19-22 degrees C) were obtained. On average about 300-500 synaptic channels were estimated to open during a sEPSC. 'Giant' sEPSCs (gsEPSCs) were also observed. The amplitudes of gsEPSCs were up to 14 times larger than the amplitude of an average normal sEPSC. Moreover, the lifetime of gsEPSCs was up to about 3 times longer than that of sEPSCs. Like sEPSCs, gsEPSCs could not be abolished by 0.1 mumol/l tetrodotoxin. The rate at which sEPSCs and gsEPSCs occurred could be markedly enhanced by serotonin (1 mumol/l) and 3,4-diaminopyridine (1 mmol/l).

4-Aminopyridine↗

Rib radiographs for trauma: useful or wasteful?

In trauma to the chest, the clinical impression and the physical findings of rib fractures are nonspecific. Fractures often are not seen on initial films. The principal diagnostic goal should be the detection of significant complications (pneumothorax, hemothorax, major vascular injury, or pulmonary contusion) requiring admission. The therapeutic effort should be to provide pain relief and prevent the delayed development of atelectasis or pneumonia in patients with painful chest wall injuries, whether or not a fracture is detected initially. An upright posteroanterior chest radiograph has the greatest yield in detecting fractures and complications resulting from them. Tomograms and expiratory, oblique, and "coned-down" views should not be done routinely. The use of these more specific examinations may be indicated, however, in such cases as trauma to ribs 1 to 3 or 9 to 12. Their selective use in isolated cases (trauma to ribs 1 to 3 or 9 to 12) and suspected child abuse may indicate the need for these more specific examinations. Because detection of pulmonary complications of chest trauma is most important, a delayed or repeat upright posteroanterior chest radiograph may be the most cost-effective second radiograph. Significant medical care cost savings may be appreciated by limiting the use of specific rib views to instances in which it might influence the patient's therapy.

Adolescent↗

Tonic depolarization of excitatory nerve terminals in crayfish muscle by high concentrations of extracellular potassium.

At voltage-clamped fibres of the claw opener muscle of small crayfish, spontaneous quantal release of excitatory transmitter elicited by raising extracellular K+ to 100 mM was investigated. On application of the high K+ concentration, the rates of quantal release increased to n = 10,000-25,000 quanta/s within 10 s, and thereafter declined exponentially, either with a single (tau congruent to 15-40 s) or with two (tau 1 congruent to 15-40 s, tau 2 greater than 70 s) time constants. The total number of quanta released per trial ranged from s = 200,000 to 800,000 quanta. The results were derived by means of the fluctuation analysis technique.

Animals↗

Excitatory transmitter release induced by high concentrations of gamma-aminobutyric acid (GABA) in crayfish neuromuscular junctions.

At the neuromuscular junction of very small crayfish (0.4-2 g) addition of gamma-aminobutyric acid (GABA) to the superfusing solution at concentrations exceeding 100 mmol/l elicited high frequency release of excitatory transmitter quanta. In seven experiments single application of 500 mmol/l GABA gave rise to instantaneous release of 70,000 to 130,000 quanta. These stores of transmitter were released by GABA in a first order process with time constants, tau q, of between 9 s and 20 s, the maximum rate of release, ñ0, reaching 10,000 quanta/s in some cases. After release had ceased in the presence of GABA, the preparation was allowed to recover for five minutes in normal solution. Subsequently, a second trial evoked about 50% of the release induced during the first application of GABA. Pretreatment of the preparation with 2 mumol/l serotonin (5-HT) facilitated GABA-induced transmitter release resulting in larger rates of release and consequently in a larger output of transmitter by a factor of about 3. The largest amount of transmitter released on a single application of GABA in the presence of serotonin comprised about 220,000 quanta with a maximum rate of release ñ0 approximately equal to 25,000 quanta/s. The release evoked by high GABA-concentrations did not depend markedly on extracellular Ca2+ or Mg2+, but required extracellular Na+. The effects induced by high concentrations of GABA on release of excitatory transmitter quanta were quantitatively similar to the effects of high glycine-concentrations on release of quanta from the inhibitory terminals (Finger 1983a, b).

Animals↗

Viscoelastic properties of setting elastomeric impression materials.

An instrument was introduced to determine the relationship between induced and permanent tensile deformation of selected elastomeric dental impression materials during and after setting. The method accurately recorded viscoelastic properties of impression materials.

Chemical Phenomena↗

Giant inhibitory miniature currents in crayfish muscle in the presence and absence of extracellular sodium and serotonin.

At opener muscles of the claw, or first walking leg of small crayfish, giant spontaneous inhibitory postsynaptic currents (gsIPSCs) were recorded. In some experiments, the rate by which they occurred could be enhanced by application of 1 mumol/l serotonin (5-HT). The largest gsIPSCs seen were at least up to ten-fold larger than normal inhibitory miniature currents. Picrotoxin (10 mumol/l) reversibly abolished the gsIPSCs. Tetrodotoxin (0.1 mumol/l) or withdrawal of Na+ from the superfusion did not abolish gsIPSCs. Decay time constants of gsIPSCs, tau(gsIPSCs), were about two-fold larger than those of nerve evoked IPSCs and of normal inhibitory miniature currents. In Na+-free superfusion tau(gsIPSCs) was larger by a factor of about 1.8 than in normal superfusion, which might be a result of inhibition of a Na+-dependent transport process for inhibitory transmitter by removal of Na+ from the incubation medium.

Animals↗

High rates of excitatory miniature currents in crayfish claw opener muscle evoked by high concentrations of gamma-aminobutyric acid (GABA) in normal and Ca2+-deficient superfusions.

High concentrations (0.5 mol/l) of the neutral amino acid GABA were used to evoke release of transmitter quanta from excitatory terminals at voltage clamped crayfish muscle fibres in normal and Ca2+-deficient superfusions. An experiment in which the release of transmitter quanta proceeded at high rates in both normal and Ca2+-deficient superfusion was analyzed in detail indicating a Ca2+-independent mechanism of release. In the normal superfusion, on application of GABA, the release rates ñ increased within a few seconds up to about 6000 quanta/s and thereafter declined exponentially with a time constant tau q = 18.5 s, most likely due to depletion of a readily releasable store of transmitter in the excitatory nerve terminals comprising at least 110,000 quanta per muscle fibre. Assuming that about 1900 excitatory synapses exist per muscle fibre [9], it results that about 58 quanta can be associated with each synapse in agreement with morphological data [15] which show that between 47-117 vesicles exist in a single glutamatergic synapse of crayfish.

Animals↗

Postsynaptic actions of ethanol and methanol in crayfish neuromuscular junctions.

Actions of ethanol and methanol on excitatory postsynaptic channels activated by quisqualate were investigated in opener muscles from the first walking leg and the claw of crayfish. Both ethanol and methanol reduced the elementary currents [i] that flow through channels operated by quisqualate in a concentration-dependent manner but did not affect the apparent mean open time, tau noise, of the channels estimated from power spectra. 0.26 mol/l ethanol, or 1 mol/l methanol, respectively, reduced [i] e-fold. Ethanol also markedly decreased the size and the decay time constant tau (sEPSCs) of spontaneous excitatory postsynaptic currents (sEPSCs). At ten fibres, on the average, 0.26 mol/l ethanol decreased tau (sEPSCs) by a factor 1.56 +/- 0.24 (SD). tau (sIPSCs) and tau noise of inhibitory postsynaptic currents apparently were not affected by ethanol. Moreover the size of elementary inhibitory postsynaptic currents did not decrease in the presence of this alcohol. Thus, in crayfish opener muscles ethanol seems to selectively depress excitatory postsynaptic currents.

Animals↗

Single synaptic channels recorded at glutamate sensitive patches on a crayfish muscle.

When a patch clamp pipette filled with 50 mumol/l glutamate was placed on a muscle fiber of the deep abdominal extensor of crayfish, in some locations current pulses were recorded which were identified as synaptic, glutamate-operated ionic channel openings. At a given site all current pulses had approximately the same amplitude. At resting potential and 19 degrees C, their mean amplitudes were 7-8 pA, corresponding to channel conductances of 70-80 pS. The distribution of open times of the channels could be described by the sum of two exponentials with time constants tau 1 of 0.3-0.5 ms for the longer, and tau 2 of 0.03-0.06 ms for the shorter component. Bursts of channel openings interrupted by gaps occurred in about 10% of the events only. The longer time constant tau 1 conforms to the channel open times estimated by noise analysis [11].

Animals↗

Glutamate-operated postsynaptic channels and spontaneous excitatory postsynaptic currents in crayfish claw opener muscle.

In opener muscle fibres of the crayfish claw excitatory postsynaptic currents activated by glutamate (1 . 10(-4)-5 . 10(-4) mol/l) were investigated by means of the noise analysis technique. For the apparent mean open time of glutamate-activated channels, tau noise = 1.15 ms +/- 0.16 (S.D., n = 24) resulted at membrane potentials between E = -60 mV and E = -100 mV, T = 20-23 degrees C. No significant voltage dependence for tau noise was observed, most likely due to the pretreatment of the fibres with 1 mumol/l concanavalin A. For the conductance, gamma, of these channels, gamma = 23.6 pS +/- 5.2 (S.D., n = 24) was found. These characteristics for glutamate-operated channels differ significantly from those observed recently in opener muscle fibres of crayfish first walking leg [13]. Similarly, different characteristics were found also for the decay time constants tau (sEPSCs) of spontaneous excitatory postsynaptic currents in the respective muscles. On average, tau (sEPSCs) was 1.3 ms +/- 0.3 (S.D., n = 11) in the claw. In the first walking leg tau (sEPSCs) was shorter by a factor of about 2.4 and in the second walking leg shorter by a factor of about 2.9, than in the claw.

Animals↗

Effects of glycine on the crayfish neuromuscular junction. I. Glycine-operated inhibitory postsynaptic channels and a glycine-effected decrease in membrane conductance.

Inhibitory postsynaptic membrane channels which are activated by glycine were investigated by means of the noise analysis technique. Dose-response curves were obtained for gamma-aminobutyric acid (GABA) in the presence and in the absence of glycine, and it was concluded that GABA and glycine are likely to activate the same receptors. However, glycine proved to have a very low affinity for the inhibitory postsynaptic receptors; this affinity was smaller than that of GABA by a factor of 1 . 10(3)-2 . 10(3). The mean open time tau of the postsynaptic Cl- channels activated by glycine at E = -100 mV and E = -60 mV membrane potentials were tau = 6.1 ms +/- 1.5 ms and tau = 17.7 ms +/- 2.2 ms, respectively. These values are in agreement with the tau obtained by activation with GABA (Dudel et al. 1980); however, on activation by glycine the potential dependence of tau was larger by a factor of 1.35. At E = -100 mV the conductance gamma of glycine-operated channels was about 3 pS which is a third of the respective conductance elicited by GABA. In the presence of high concentrations of glycine (0.1-0.5 mol/l) spontaneous inhibitory postsynaptic currents (sIPSCs) and 'giant' spontaneous inhibitory postsynaptic currents (gsIPSCs) were observed. Furthermore at high concentrations of glycine an additional glycine-induced noise component was found in the power spectra of current fluctuations at higher frequencies. It was concluded that this spectral component resulted from the closing of otherwise open K+ channels, as has been observed already on application of GABA (Dudel and Finger 1980). The mean duration of the low conductance state was tau- = 2.2 ms +/- 0.9 ms and the conductance decrease gamma- coupled to this process was estimated to be about 3 pS. In Na+ free- and Ca2+-enriched bathing solutions the glycine-induced conductances gamma and gamma- were reduced by a factor of about 1.7 while tau and tau- remained unchanged. The decrease in gamma and gamma- was most likely effected by the increase in concentration of divalent cations.

Animals↗

Effects of glycine on the crayfish neuromuscular junction. II. Release of inhibitory transmitter activated by glycine.

Glycine applied in the bathing medium at concentrations exceeding 0.1 mol/l elicited high rates of spontaneous inhibitory postsynaptic currents (sIPSCs) in crayfish neuromuscular junctions. This effect of glycine was reversible within seconds. In several experiments on application of 0.5 mol/l glycine the rate of sIPSCs immediately increased to about 10 kHz and thereafter declined exponentially with time constants of between 10 and 20 s. This resulted in a release of about 140,000-200,000 inhibitory quanta per trial. When the readily releasable pool of transmitter had been so depleted by glycine, it was necessary to superfuse the preparation with normal solution for 5-10 min in order to be able to again evoke a high rate of sIPSCs. A similar effect of glycine on spontaneous release was also observed in some preparations which had been previously bathed in zero Ca2+ solution for up to 45 min. Addition of 25 mmol/l Mg2+ to the bathing fluid did not block the glycine evoked release of transmitter. However, in sodium-free superfusions the increase in the rate of sIPSCs induced by glycine was reduced. In the presence of 0.5 mol/l glycine no excitatory miniature currents (sEPSCs) were observed, in fact, glycine depressed excitatory synaptic transmission. In addition to the increasing the rate of sIPSCs, high concentrations of glycine evoked 'giant' sIPSCs (gsIPSCs). They were about 10-15 times larger than the normal sIPSCs and occurred at rates lower than 3 Hz, irrespective of whether the bathing medium contained sodium or not. However, in sodium-free superfusions the time constants of the decay of gsIPSCs were prolonged by a factor 2-3. These results suggest that glycine elicited sIPSCs and gsIPSCs by different mechanisms. Possible mechanisms which might explain the effects of glycine on release of inhibitory transmitter are discussed.

Animals↗