Abstract
Paired‐pulse depression (PPD), a short‐term neural plasticity, was studied in hippocampal CA1 of urethane‐anesthetized rats in vivo, using field potential recordings and current source density analysis. PPD was robust when an ipsilateral CA3 (iCA3) conditioning pulse of moderate stimulus intensity was followed 30–200 ms later by a contralateral CA3 (cCA3) test pulse; the ratio of the conditioned (C) to the nonconditioned (NC) response, as measured by the peak excitatory sink at the apical dendrites, ranged from 0.6 to 0.8. An alveus conditioning pulse evoked a large antidromic population spike in CA1 and a modest depression of the CA3‐evoked excitatory sink (C/NC ratio of ∼0.85). High‐intensity paired pulses, both delivered to iCA3, also showed PPD of the proximal excitatory sinks; however, paired‐pulse facilitation of the dendritic sinks was found at the mid‐apical dendrites, >250 μm from the soma. Local injection of GABA~A~ antagonist picrotoxin or bicuculline increased the C/NC ratio at IPIs of <150 ms, as well as the ratio of the amplitude of the population spikes (P2/P1; where P2 and P1 are the population spikes evoked by the second and first pulse, respectively). GABA~B~ receptor antagonists, CGP35348 given intracerebroventricularly or CGP56999A administered locally, increased C/NC and P2/P1 at IPIs of 150–400 ms. It is concluded that conditioned depression of the excitatory sinks was caused by mainly feedforward and some feedback inhibition at the apical dendrites. GABA~A~‐mediated postsynaptic inhibition dominated at early latencies, while GABA~B~‐mediated inhibition prevailed at long latencies, probably at both presynaptic and postsynaptic sites. PPD of the excitatory sinks provides a measure of population dendritic inhibition in vivo. © 2008 Wiley‐Liss, Inc.