Regulation of Glycinergic mIPSCs by Ca and K Channels on Nerve Endings.

Abstract

More than 70 different K⁺ channel subunits have been identified and their molecular structure and diversity were investigated over the past 15 years, though K⁺ channel subtypes less than 10 are known as native functional ones. Furthermore, the study of K⁺ channels on the presynaptic nerve endings had been quite limited in the a few huge nerve endings such as basket cell terminals and Calyx of Held on the hearing pathway where direct approach of patch pipette is possible. Therefore, we investigated the functional K⁺ channels on the small nerve endings having less than 1µm diameter of glycinergic interneurons projecting to spinal sacral dorsal commissural nucleus (SDCN) neurons. In the presence of TTX, whole-cell patch recording of mIPSCs was made using SDCN ‘synaptic bouton ’preparation attached with functional glycinergic nerve at a holding potential of 0mV. Glutamatergic and GABAergic inputs were inhibited by CNQX, AP-5 and bicuculline. The K⁺ channel blockers, 4-AP, TEA, δ-Dendrotoxin, Iberiotoxin, Charybdotoxin and Apamin increased considerably mIPSCs frequency without affecting the amplitude.Consequently, the existence of following K⁺ channel subtypes on nerve endings was estimated: i.e., KA > KIR > IKCa > BKCa. As Ca²⁺ channels on glycinergic nerve endings, L-, N-, P/Q- and R types were recognized using respective channel blockers: i.e., nifedipine, ω-CgTX, AgTX, Cd²⁺, though heterogeneous distribution of these Ca²⁺ channel subtypes was found among preparations tested. [Jpn J Physiol 55 Suppl:S123 (2005)]