Cyclic Nucleotides Induce Long-Term Augmentation of Glutamate-Activated Chloride Current in Molluscan Neurons
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Literature data indicate that serotonin induces the long-term potentiation of glutamate (Glu) response in molluscan neurons. The aim of present work was to elucidate whether cyclic nucleotides can cause the same effect.
Experiments were carried out on isolated neurons of the edible snail (Helix pomatia) using a two-microelectrode voltage-clamp method.
In the majority of the cells examined, the application of Glu elicited a Cl−-current. The reversal potential (Er) of this current lied between −35 and −55 mV in different cells.
Picrotoxin, a blocker of Cl−-channels, suppressed this current equally on both sides of Er. Furosemide, an antagonist of both Cl−-channels and the Na+/K+/Cl−-cotransporter, had a dual effect on Glu-response: decrease in conductance, and shift of Er to negative potentials.
A short-term (2 min) cell treatment with 8-Br-cAMP or 8-Br-cGMP caused long-term (up to 30 min) change in Glu-response. At a holding potential of −60 mV, which was close to the resting level, an increase in Glu-activated inward current was observed. This potentiation seems to be related to the right shift of Er of Glu-activated Cl−-current rather than to the increase in conductance of Cl−-channels. The blocking effect of picrotoxin rested after 8-Br-cAMP treatment.
The change in the Cl−-homeostasis as a possible mechanism for the observed effect of cyclic nucleotides is discussed.
Keywordscyclic AMP cyclic GMP potentiation glutamate response chloride current molluscan neurons
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