title: NMDA receptor-mediated depolarizing after-potentials in the basal dendrites of CA1 pyramidal neurons.
abstract: It was shown recently that the basal dendrites of cortical pyramidal neurons generate NMDA-spikes. In the present study, we made whole-cell recordings from hippocampal CA1 pyramidal neurons and examined whether NMDA receptor activation was involved in synaptic responses. At low input stimulus intensity, EPSPs with a fast decay time were induced. As the intensity of stimulation was increased in the presence of GABA receptor antagonists, a depolarizing after-potential (DAP) was generated in addition to a fast decaying potential. A DAP was never observed when the input was applied to the apical dendrites. The DAP was suppressed by hyperpolarization or by NMDA receptor antagonists, but not by Na+, K+, or Ca2+ channel blockers. One possible mechanism is that the morphology of the basal dendrites favors DAP generation. A compartmental model simulation showed that synaptic inputs to thinner shorter dendrites generated a potential that resembled a DAP. Our study shows that a synaptic input to the basal dendrites of a hippocampal pyramidal neuron can generate a NMDA receptor-mediated potential in the presence of GABA receptor blockade.
authors.affiliation: Laboratory of Cellular Neurobiology, School of Life Science, Tokyo University of Pharmacy and Life Science, Hachioji, Tokyo 192-0392, Japan.
authors.forename: Ryosuke
authors.initials: R
authors.lastname: Enoki
authors.forename: Teppei
authors.initials: T
authors.lastname: Kiuchi
authors.forename: Amane
authors.initials: A
authors.lastname: Koizumi
authors.forename: Go
authors.initials: G
authors.lastname: Sasaki
authors.forename: Yoshihisa
authors.initials: Y
authors.lastname: Kudo
authors.forename: Hiroyoshi
authors.initials: H
authors.lastname: Miyakawa
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002478:Cells, Cultured; D003712:Dendrites / Q000502:physiology* / Q000528:radiation effects; D004558:Electric Stimulation / Q000379:methods; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology*; D018756:GABA Antagonists / Q000494:pharmacology; D005711:Gallopamil / Q000031:analogs & derivatives* / Q000494:pharmacology; D006624:Hippocampus / Q000166:cytology*; D008012:Lidocaine / Q000031:analogs & derivatives* / Q000494:pharmacology; D008297:Male; D008959:Models, Neurological; D018408:Patch-Clamp Techniques / Q000379:methods; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology* / Q000528:radiation effects; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists / Q000502:physiology*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D018709:Statistics, Nonparametric; D014633:Valine / Q000031:analogs & derivatives* / Q000494:pharmacology
chemical_list: D002121:Calcium Channel Blockers; D018756:GABA Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; D026941:Sodium Channel Blockers; C012647:QX-314; D005711:Gallopamil; C056639:2-amino-5-phosphopentanoic acid; C041386:D 890; D008012:Lidocaine; D014633:Valine