The synaptically evoked late hyperpolarisation in hippocampal CA1 pyramidal cells is resistant to intracellular EGTA.
It has been suggested that the late hyperpolarisation following synaptic activation of hippocampal CA1 pyramidal neurons is activated by calcium influx. This hypothesis was examined using microelectrodes containing EGTA. Intracellular injection of EGTA blocked the afterhyperpolarisation which normally followed cell firing produced by injection of a depolarising current or the ionophoresis of glutamate onto the apical dendrites. In contrast, the hyperpolarisation following synaptic activation was resistant to EGTA. The results suggest that this potential is not dependent on intracellular Ca2+. Other possible mechanisms are discussed.
D000818:Animals; D002118:Calcium / Q000502:physiology; D004533:Egtazic Acid / Q000494:pharmacology*; D004594:Electrophysiology; D005026:Ethylene Glycols / Q000494:pharmacology*; D005971:Glutamates / Q000494:pharmacology; D006624:Hippocampus / Q000166:cytology / Q000502:physiology*; D007267:Injections; D007425:Intracellular Membranes; D009474:Neurons / Q000502:physiology; D051381:Rats; D013569:Synapses / Q000502:physiology*
D005026:Ethylene Glycols; D005971:Glutamates; D004533:Egtazic Acid; D002118:Calcium