Kayoko Onodera

Effects of kainic acid on the glutamate receptors of the crayfish muscle

The effect of kainic acid on the action of l-glutamate on the crayfish muscle was investigated. l-Glutamate was applied iontophoretically and potential changes were recorded intracellularly. Kainic acid was then added to the bath solution. When the peak time of the glutamate potential was less than about 50–100 msec, kainic acid (10−4 M) had little or no effect on the amplitude. However, when the peak time of the glutamate potential was about 800 msec, kainic acid increased the amplitude of the glutamate potential to three times that of the control. The glutamate potential was, in many cases, prolonged by the action of kainic acid. When the amplitude distribution of the glutamate potential was measured by injecting the same doses of l-glutamate along a muscle fibre, the area sensitive to l-glutamate was larger in kainic acid solution than in the normal solution. It is suggested that sensitivity of the junctional receptor is not changed by the action of kainic acid, but the extra-junctional receptor, which is not responsive to l-glutamate in the normal solution becomes sensitive to l-glutamate by kainic acid.

Inhibitory effect of streptomycin and related antibiotics on the glutamate receptor of the crayfish neuromuscular junction

Abstract The effect of streptomycin, kanamycin and neomycin on the neuromuscular junction of the crayfish was investigated. Bath application and iontophoretic application of streptomycin depressed the excitatory postsynaptic potential (EPSP) and the glutamate potential. The degree of depression of the EPSP by the action of streptomycin was almost the same as that of the glutamate potential. The inhibitory postsynaptic potential and the γ-aminobutyric acid potential were not changed by strep tomycin. Similar but slightly smaller effects were observed with kanamycin and neomycin. The number of quanta released per impulse was estimated by recording the extracellular EPSP. The quantum content remained almost unchanged during the action of streptomycin, while the quantum size was decreased. The dose-response relationship of l -glutamate estimated from the iontophoretic application was depressed by streptomycin with no apparent parallel shift of the curve. These results suggest that streptomycin acts on the excitatory postsynaptic membrane and depresses the glutamate receptor but shows no effect on the γ-aminobutyric acid receptor.

L-Glutamic acid as an excitatory transmitter at the crayfish neuromuscular junction.

Abstract 1. Release of glutamate and aspartate from the crayfish muscle was measured by mass fragmentography. 2. Nerve stimulation significantly increased glutamate efflux, but the change in aspartate efflux was very small and not significant. 3. Black widow spider venom (BWSV) increased the frequency of miniature EPSPs and the efflux of glutamate. 4. These results provide further evidence for the glutamate-transmitter hypothesis.