A postsynaptic excitatory amino acid transporter with chloride conductance functionally regulated by neuronal activity in cerebellar Purkinje cells.
Excitatory amino acid (EAA) neurotransmitters induce postsynaptic depolarization by activating receptor-mediated cation conductances, a process known to underlie changes in synaptic efficacy. Using a patch-clamp method, we demonstrate here an EAA-dependent postsynaptic anion conductance mediated by EAA transporters present on cerebellar Purkinje cell bodies and dendrites in culture. This transporter-mediated current was modulated by neuronal activity: it exhibited facilitation for >20 min after transient depolarization accompanied by Ca2+ influx. Evidence is presented suggesting that the transporter facilitation is mediated by arachidonate release after Ca2+-dependent activation of phospholipase A2, which exists in Purkinje cells. This postsynaptic reuptake system may represent a novel modulatory mechanism of synaptic transmission as well as prevent neuronal excitotoxicity.
Kataoka
Y
Y
Department of Neuroscience, Osaka Bioscience Institute, Osaka 565, Japan.
Morii
H
H
Watanabe
Y
Y
Ohmori
H
H
D000818:Animals; D016718:Arachidonic Acid / Q000494:pharmacology; D001224:Aspartic Acid / Q000494:pharmacology; D001693:Biological Transport, Active; D018118:Chloride Channels / Q000378:metabolism*; D018846:Excitatory Amino Acids / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D011689:Purkinje Cells / Q000378:metabolism*; D051381:Rats; D017981:Receptors, Neurotransmitter / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects
D018118:Chloride Channels; D018846:Excitatory Amino Acids; D017981:Receptors, Neurotransmitter; D016718:Arachidonic Acid; D001224:Aspartic Acid