Fig. 6

AMPA-mediated currents evoked by neuron activity drive AP firing in pre-OLs. a Representative trace of synaptic currents evoked by glutamate application (1 mM) in an excitable pre-OL during voltage-clamp recording (P10). CNQX (50 µM; AMPAR blocker) largely reduced the synaptic current; additional application of Naspm (50 µm; Ca²⁺-permeable AMPAR blocker) abolished most of the remaining current. b Summary of glutamate receptor-mediated synaptic currents in the presence of CNQX and Naspm. c Representative trace of glutamate-evoked depolarization and firing in an excitable pre-OL in a current-clamp recording. Application of CNQX blocked nearly all depolarization and subsequent spikes. Inset, expanded time scales of APs. d Summary of membrane potential changes upon glutamate application in the presence of CNQX and Naspm. Data represent the mean ± s.e.m.; *P < 0.05, ***P < 0.0001. e Immunostaining of CNPase-eGFP+ cells with antibodies against calretinin (Ca²⁺-bind protein as a marker for axon fibers, red) and Na_v1.2 (blue) in the MNTB (P14). Note that processes of CNPase-eGFP+ cells make contact with axon fibers. Scale bar, 10 μm. f Glutamate-mediated synaptic currents evoked by axon fiber stimulation (100 Hz, 1 s; see diagram) in an excitable pre-OL (P11). CNQX blocked the synaptic current. g Depolarization and firing activity evoked by electrical stimulation (100 pulses at 100 Hz) in a current-clamp recording of an excitable pre-OL. Inset, expanded time scales of an AP indicated in the box. Application of μ-conotoxin KIIIA (1 μM) completely blocked firing activity, and additional application of CNQX (50 μM) significantly reduced depolarization. Dashed lines indicate membrane potential. Red arrows indicate the end time point of the afferent fiber simulation