Biomedical subjects

K T Wann

Publications and source records attributed to K T Wann.

34 records · Page 2Linked to original sources

PubMed1984

The effect of temperature on the growth and decay times of miniature end-plate currents in the mouse diaphragm.

The temperature dependence of both the growth and the decay phases of miniature end-plate currents was investigated in the mouse diaphragm. The relationship between the log of the time constant of decay and reciprocal temperature was linear, that between the growth phase duration and temperature was not linear, the Q10 being higher over the low end of the temperature range. The possible reasons for the non-uniform Q10 of the growth time of the miniature end-plate current are discussed.

Animals↗

PubMed1984

Hydrostatic pressure modifies the action of octanol and atropine on frog endplate conductance.

The effects of octanol, ethanol and atropine were examined on the time course of decay (tau D) of miniature endplate currents (m.e.p.cs) in the frog neuromuscular junction at normal and high pressure. Octanol (25-100 microM) decreased reversibly the tau D of m.e.p.cs in a dose-dependent manner, 100 microM reducing tau D to 0.39 of the control value. Higher concentrations (200-500 microM) additionally depressed the amplitude of m.e.p.cs. Hydrostatic pressure (3.19 and 5.25 MPa) reduced the tau D of octanol (25-100 microM)-shortened m.e.p.cs. Thus 3.19 MPa and 5.25 MPa reduced the tau D in the presence of 100 microM octanol to 0.75 and 0.78 of the octanol treated values. This effect was not completely reversed on decompression. The m.e.p.c. amplitude is reversibly decreased by pressure in the presence of octanol. Hydrostatic pressure (3.19-15.55 MPa) did not modify the effect of ethanol on tau D. At 10.40 and 15.55 MPa the tau D was increased equally in the absence or presence of ethanol. Atropine (60 microM) reduced the tau D and amplitude of m.e.p.cs to 0.33 and 0.63 of the control values. These effects were completely reversible. Hydrostatic pressure (3.19 and 5.25 MPa) reduced the tau D of atropine-shortened m.e.p.cs to 0.82 and 0.77 of the atropine-treated values respectively. This effect was not completely reversed on decompression. Hydrostatic pressure also reversibly depressed the amplitude of atropine-treated m.e.p.cs. The implications of these drug-hydrostatic pressure interactions are discussed.

1-Octanol↗

PubMed1983

Extracellular chloride replacement by isethionate induces abnormal spontaneous release of transmitter at the frog neuromuscular junction.

1 Replacement of chloride by isethionate in Ringer solution bathing frog skeletal muscle fibres induces, after a delay of about 30 min, marked mechanical activity which was blocked by tubocurarine. This effect is reversed by washing out the isethionate. 2 Miniature end plate potentials (m.e.p.ps) and giant potentials (potentials greater than or equal to 2 X modal value) were recorded intracellularly in normal Ringer and isethionate Ringer solution. 3 The frequency of m.e.p.ps was unaltered by isethionate. The proportion of giant potentials increased from 3% in normal Ringer to 24.5% in isethionate Ringer after 90 min. This effect is usually reversible if the exposure to isethionate does not exceed 2 h. 4 The giant potentials were large enough to initiate trains of action potentials and still occurred in the presence of tetrodotoxin or Ca2+-free Ringer. Isethionate produced no change in the tau D of miniature endplate currents. 5 Chloride replacement by propionate produced no change in the proportion of giant potentials. 6 It is suggested that the isethionate anion can induce giant potentials and the possible mechanism of action is discussed.

Alkanesulfonates↗

PubMed1983

The effect of temperature on the nerve-blocking action of benzyl alcohol on the squid giant axon.

The action of benzyl alcohol was studied on the voltage-clamped giant axons of Loligo forbesi. The depressant effect of 7.5 mM-benzyl alcohol on the action potential amplitude and peak rate of rise was more marked at a low (8 degrees C) than at a high temperature (16.5 degrees C). A small depolarization (approximately 5 mV) was also produced. These effects were usually reversible. Benzyl alcohol (7.5 mM) selectively depressed the amplitude of the peak early current. The maximum inward current was depressed to 0.65 and 0.67 of the control value at 20 degrees C and 7 degrees C respectively. This effect was usually reversible. Benzyl alcohol also depressed the peak inward conductance (gNa but had no effect on the time to peak early current. A small reversible decrease in the time constant of inactivation (tau h) was caused by benzyl alcohol (7.5 mM). This was usually reversible on washout of the anaesthetic. Benzyl alcohol (7.5 mM) had no effect on the time course of activation or the amplitude of the delayed outward current. The curve of the steady-state inactivation parameter (h infinity) for the Na current against the conditioning membrane potential was shifted by benzyl alcohol in a hyperpolarizing direction (at h infinity = 0.5 the shift was an average of 3.3 mV and was reversible). Increasing the temperature from 7 to 20 degrees C shifted the curve in a depolarizing direction by approximately 10 mV. The reason for the increased nerve-blocking action of benzyl alcohol at the lower temperature is discussed.

Action Potentials↗

PubMed1982

The effects of hydrostatic pressure on the spontaneous release of transmitter at the frog neuromuscular junction.

1. The effects of hydrostatic pressure (0.1-15.55 MPa) on the spontaneous release of transmitter at the frog neuromuscular junction were investigated. 2. The major effect of high pressure is on the release mechanism, pressure (0.1-10.40 MPa) producing an exponential decrease in frequency of the miniature end-plate currents in normal Ringer solution. The frequency decreases to 0.52 and 0.24 of the control value at 5.25 and 10.40 MPa respectively. This effect is reversible on decompression. 3. The sensitivity of the release process to high pressure is unaltered in 10 mM-K+, 6 mM- and 10 mM-Ca2+ and hypertonic (165 mM-NaCl) Ringer solution, although the high Ca2+ media shift the threshold for the pressure effect to higher pressures. 4. Higher pressure (10.40-15.55 MPa) produces a small increase in the time constant of decay (tau D) of m.e.p.c.s with no effect on the growth phase. A pressure of 15.55 MPa increases tau D to 1.35 of the control value. 5. The possible actions of high pressure on both the pre- and post-synaptic processes are briefly discussed.

Animals↗

PubMed1981

The action of high hydrostatic pressure on the membrane currents of Helix neurones.

1. The actions of high hydrostatic pressure (10.4, 20.8 MPa) on the membrane currents of Helix neurones were examined under voltage clamp. 2. High hydrostatic pressure (20.8 MPa) reduced the maximum inward current to 0.78 and the delayed outward current, measured at the inward current reversal potential, to 0.75 of their value at atmospheric pressure. 3. High hydrostatic pressure shifted the curve relating the inward current conductance to membrane potential to more positive values but the maximum conductance was altered. 4. The rates of activation of the inward and delayed outward currents were slowed by pressure. 5. The steady-state level and time course of inactivation of the inward current was unaffected by high pressure over the investigated range. 6. The effects of high hydrostatic pressure on the fast outward current identified in gastropod neurones by Connor & Stevens (1971) were also examined. 20.8 MPa reduced the current measured at -30 mV to 0.71 of its control value. 7. The rate of activation of the fast outward current was slowed by high pressure but the time constant of inactivation was unchanged. 8. The majority of the effects of high hydrostatic pressure were completely reversible upon decompression. 9. These results are discussed with reference to the known effects of high hydrostatic pressure on the action potential and discharge frequency of gastropod neurones. Possible sites and mechanisms of pressure action on the excitable cell are briefly discussed.

Action Potentials↗

PubMed1979