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. 2008 Feb 20;28(8):1804–1815. doi: 10.1523/JNEUROSCI.4616-07.2008

Figure 9.

Figure 9.

Isoproterenol-induced depression of coupling functionally affects propagation of GABAA receptor-mediated postsynaptic currents. A, Cartoon showing the experimental configuration. Direct GABAA receptor-mediated input on the recorded neuron (left, gray indicates the high-chloride intracellular solution used) has an estimated reversal potential (Erev1) of 0 mV. In contrast, gap junction-propagated input (right) has a lower (less than −15 mV) reversal potential (Erev2) (Vh, holding potential). B, Spontaneous synaptic events of opposite polarities recorded with chloride-loaded electrodes in the presence of blockers of glutamatergic and GABAB-mediated synaptic transmission: notice that both type of events are sensitive to the GABAA receptor antagonist gabazine (Gbz) (12.5 μm). Because of the relatively rare occurrence of outward compared with inward events, sweeps were selected from noncontiguous epochs. C, Isoproterenol (Iso) (10 μm) selectively reduces the frequency of outward events. For the same reasons expressed above, noncontiguous traces are shown in the figure. D, Summary graphs from n = 8 experiments. Notice that isoproterenol does not affect the peak amplitude of either inward (white circles) or outward (black circles) currents. In contrast to inward currents (black squares), notice the selective depression of the frequency of outward events (white squares). Summary plots showing the time course of the effect of isoproterenol on normalized peak amplitude and frequency are shown at the left, whereas graphs of the absolute values are illustrated at the right (Ctrl, control; Iso, isoproterenol).