Figure 2
Whole cell patch clamp recordings of spontaneous GABA-mediated inhibitory postsynaptic currents (IPSC) in CA1 neurons revealed two sites of action for anesthetic-induced enhanced inhibition. (A) Spontaneous synaptic currents were blocked by a GABAA-receptor antagonist bicuculline (BIC), indicating that they were GABAA-mediated Cl- currents. Traces on the top show 20 s of continuous recording from a CA1 neuron in control and in the presence of BIC. A rate meter graph (bottom) shows the relatively stable frequency of IPSCs during 20 min of control recording, followed by a rapid and complete block of responses produced by BIC (indicated by the bar). (B) Halothane produced a marked increase of the inhibitory charge transfer in CA1 neurons measured as the integral of current recordings (shaded area in top traces). A three fold increase of inhibitory charge (pico Colombs – pC) was reversibly produced by halothane and appeared to come about through both a prolongation of IPSC time course (C) and from an increased frequency of synaptic currents (D). Both effects persisted in the presence of 10 μM tetrodotoxin (TTX) and/or glutamate receptor antagonists indicating that action potential dependent activity and glutamate synapses were not required for anesthetic action. For the rate meter histograms in (A) and (D), each bin represents the number of events recorded in 4 s divided by 4 to give a frequency in Hz (events/second). For all IPSC recordings a CsCl based internal solution was used in the patch pipette.