1. The effects of octanol, ethanol and atropine were examined on the time course of decay (tD) of miniature endplate currents (m.e.p.cs) in the frog neuromuscular junction at normal and high pressure.
2. Octanol (25-100 µM) decreased reversibly the tD of m.e.p.cs in a dose-dependent manner, 100 µM reducing tD to 0.39 of the control value. Higher concentrations (200-500 µM) additionally depressed the amplitude of m.e.p.cs.
3. Hydrostatic pressure (3.19 and 5.25 MPa) reduced the tD of octanol (25-100 µM)-shortened m.e.p.cs. Thus 3.19 MPa and 5.25 MPa reduced the tD in the presence of 100 µM 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.
4. Hydrostatic pressure (3.19-15.55 MPa) did not modify the effect of ethanol on tD. At 10.40 and 15.55 MPa the tD was increased equally in the absence or presence of ethanol.
5. Atropine (60 µM) reduced the tD 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 tD 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.
6. The implications of these drug-hydrostatic pressure interactions are discussed.
|Number of pages||8|
|Journal||British Journal of Pharmacology|
|Publication status||Published - Oct 1984|
- Rana pipiens
- Neuromuscular Junction
- Rana temporaria
- Hydrostatic Pressure
- Motor Endplate
- Neural Conduction