title: TEA-induced long-term potentiation at hippocampal mossy fiber-CA3 synapses: characteristics of its induction and expression.
abstract: Potassium ion channel blockade by tetraethylammonium (TEA) reportedly induces long-term potentiation (LTP) at hippocampal mossy fiber (MF)-CA3 synapses, but the characteristics of induction, expression, and modulation of the LTP remain unclear. In the present study, these features of TEA-induced LTP at MF-CA3 synapses were electrophysiologically examined using rat hippocampal slices. Synaptic responses recorded from MF-CA3 synapses were enhanced long-term by TEA application even under the blockade of NMDA receptors with D-AP5, whereas selective pharmacological blockade of T-type voltage-dependent calcium channels (VDCCs) strongly inhibited TEA-induced LTP. Decrease of the paired-pulse facilitation ratio after LTP induction by TEA suggests the involvement of increased neurotransmitter release probability from MF terminals as LTP expression. The facilitative modulation of MF-CA3 LTP by GABA(A) receptor activation reported previously was reversed when bumetanide, a blocker of Na(+)-K(+)-Cl(-) co-transporters (NKCCs), was applied, suggesting that the region-specific modulation of TEA-induced LTP by GABAergic inputs at MF-CA3 synapses is due to the dominance of NKCC action at MF terminals.
authors.affiliation: Department of Psychology, Graduate School of the Humanities, Senshu University, 2-1-1 Higashimita, Tama-ku, Kawasaki, Kanagawa 214-8580, Japan.
authors.forename: Etsuko
authors.initials: E
authors.lastname: Suzuki
authors.forename: Takashi
authors.initials: T
authors.lastname: Okada
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020747:Calcium Channels, T-Type / Q000187:drug effects / Q000378:metabolism; D058785:GABA-A Receptor Agonists; D006624:Hippocampus / Q000187:drug effects* / Q000502:physiology; D017774:Long-Term Potentiation / Q000187:drug effects* / Q000502:physiology; D008297:Male; D019599:Mossy Fibers, Hippocampal / Q000187:drug effects* / Q000502:physiology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D009924:Organ Culture Techniques; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology*; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011963:Receptors, GABA-A / Q000378:metabolism; D049994:Sodium Potassium Chloride Symporter Inhibitors; D028021:Sodium-Potassium-Chloride Symporters / Q000378:metabolism; D064506:Solute Carrier Family 12, Member 2; D013569:Synapses / Q000187:drug effects* / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology; D019789:Tetraethylammonium / Q000494:pharmacology*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D002121:Calcium Channel Blockers; D020747:Calcium Channels, T-Type; D058785:GABA-A Receptor Agonists; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D011963:Receptors, GABA-A; C578879:Slc12a2 protein, rat; D049994:Sodium Potassium Chloride Symporter Inhibitors; D028021:Sodium-Potassium-Chloride Symporters; D064506:Solute Carrier Family 12, Member 2; D005680:gamma-Aminobutyric Acid; D019789:Tetraethylammonium