Especially in arthropod glutamatergic synaptic systems, microM l-glutamate (Glu) concentrations often elicit Cl- currents, in addition to the excitatory cationic currents that are triggered by much higher Glu concentrations. In crayfish, Ibotenate (Ibo) is a specific agonist of the Glu-ergic Cl- currents. Application of Glu to Glu-transporters opens associated Cl- currents that inhibit quantal release presynaptically and by occupying the transporter prevents removal of released Glu. The latter prolongs the decay of postsynaptic EPSCs. It was tested whether the Ibo-elicited Cl- currents show the same pre- and post-synaptic effects as the transporter elicited ones, suggesting that also this current component arises through transporter activation. Indeed, Ibo applied to single synaptic junctions produced inhibition of quantal release and prolongation of EPSCs, very similar to the effects of Glu. It seems probable, therefore, that at least in crayfish Glu-ergic Cl- currents are generated by activation of transporters. Since generally such transporters are located around Glu-ergic synapses, this is likely to be a general mechanism. The toxin Ivermectin also elicits Cl- currents. However, while Ivermectin inhibits release too, it does not prolong the decay of EPSCs and is probable to activate GABAergic channels.     «

Especially in arthropod glutamatergic synaptic systems, microM l-glutamate (Glu) concentrations often elicit Cl- currents, in addition to the excitatory cationic currents that are triggered by much higher Glu concentrations. In crayfish, Ibotenate (Ibo) is a specific agonist of the Glu-ergic Cl- currents. Application of Glu to Glu-transporters opens associated Cl- currents that inhibit quantal release presynaptically and by occupying the transporter prevents removal of released Glu. The latter p...     »