Anomalous voltage dependence of channel blockade at a crustacean glutamate-mediated synapse.

AUTOR(ES)

Lingle, C J

RESUMO

1. The voltage dependence and concentration dependence of blockade of glutamate-activated currents by the diquaternary amine, chlorisondamine, were examined in a marine crustacean muscle. 2. Chlorisondamine results in the splitting of focally recorded synaptic current decays into two exponential components. The fast component becomes faster with increases in drug concentration and with hyperpolarization. The slow decay rate is unchanged or faster with hyperpolarization and the relative amplitude of the slow component is increased with hyperpolarization. 3. The alteration of synaptic current decay rates by chlorisondamine over the range of 5 to 100 microM and -80 to -140 mV is quantitatively consistent with a simple channel blockade model with a zero-voltage blocking rate of 6 x 10(5) M-1 s-1 at 12 degrees C with a voltage dependence of about 40 mV per e-fold change. The unblocking rate is about 5 s-1 at 0 mV and increases with hyperpolarization with a voltage dependence of about 30 mV per e-fold change. 4. The dose dependence and voltage dependence of blockade of ionophoretically activated glutamate currents by chlorisondamine are qualitatively consistent with the kinetic estimates. 5. The anomalous voltage dependence of the unblocking process is considered in terms of the possibility that the relief from blockade by chlorisondamine occurs by transit of chlorisondamine through the ion channel opened by glutamate.

Documentos Relacionados

• Activation of protein kinase C promotes glutamate-mediated transmission at the neuromuscular junction of the mealworm.
• Ganglioside inhibition of glutamate-mediated protein kinase C translocation in primary cultures of cerebellar neurons.
• Activation of a caspase 3-related cysteine protease is required for glutamate-mediated apoptosis of cultured cerebellar granule neurons
• Voltage-clamp analysis of a crayfish rectifying synapse.
• Long-term activation of adenosine receptors regulates the survival and blocks glutamate-mediated neurotoxicity in cultures of retinal neurons