TY - JOUR T1 - Activity-Dependent Maintenance of Long-Term Potentiation at Visual Cortical Inhibitory Synapses JF - The Journal of Neuroscience JO - J. Neurosci. SP - 7539 LP - 7546 DO - 10.1523/JNEUROSCI.20-20-07539.2000 VL - 20 IS - 20 AU - Yukio Komatsu AU - Yumiko Yoshimura Y1 - 2000/10/15 UR - http://www.jneurosci.org/content/20/20/7539.abstract N2 - Neural activity producing a transient increase in intracellular Ca2+ concentration can induce long-term potentiation (LTP) at visual cortical inhibitory synapses similar to those seen at various excitatory synapses. Here we report that low-frequency neural activity is required to maintain LTP at these inhibitory synapses. Inhibitory responses of layer 5 cells evoked by layer 4 stimulation were studied in developing rat visual cortical slices under a pharmacological blockade of excitatory synaptic transmission using intracellular and whole-cell recording methods. Although LTP induced by high-frequency stimulation (HFS) persisted while test stimulation was applied at 0.1 Hz, it was not maintained in approximately two-thirds of cells after test stimulation was stopped for 30 min. In the rest of the cells, LTP seemed to be maintained by spontaneous presynaptic spikes, because presynaptic inhibitory cells discharged spontaneously in our experimental condition and because LTP was totally abolished by a temporary application of Na+ channel blockers. Experiments applying various Ca2+ channel blockers and Ca2+ chelators after HFS demonstrated that LTP maintenance was mediated by presynaptic Ca2+ entries through multiple types of high-threshold Ca2+channels, which activated Ca2+-dependent reactions different from those triggering transmitter release. The Ca2+ entries associated with action potentials seemed to be regulated by presynaptic K+ channels, presumably large-conductance Ca2+-activated K+ channels, because the application of blockers for these channels facilitated LTP maintenance. In addition, noradrenaline facilitated the maintenance of LTP. These findings demonstrate a new mechanism by which neural activity regulates the continuation and termination of LTP at visual cortical inhibitory synapses. ER -