Figure 4.

Population spike depression produced by pentobarbital was partially mediated by enhanced GABA_A receptor gated chloride channels, but GABA_B receptors and non-synaptic effects did not appear to play any role. A concentration of 400 μM pentobarbital was sufficient to produce complete depression of first and second pulse population spike responses. The GABA_A receptor antagonist, bicuculline partially reversed the depression for both paired pulse responses (A). The GABA_B receptor antagonist, CGP 35348 did not reverse any of the pentobarbital-induced depression, even in the presence of supra-maximally effective concentrations of the antagonist (10 μM; B). The chloride channel blocker, picrotoxin, produced a similar – but not identical – degree of reversal of the pentobarbital-induced depression of population spike responses (C). Changes in postsynaptic excitability of CA1 neurons did not appear to play a major role in the pentobarbital-induced depression, since only a small depression of antidromically-evoked population spike responses was evident at concentrations that produced complete depression of orthodromically-evoked responses (D), and all of this depression was reversed by picrotoxin. Symbols represent the mean ± SD for at least five time matched experiments from separate brain slices.