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. 2020 Jul 1;30(12):6135–6151. doi: 10.1093/cercor/bhaa159

Figure 2.

Figure 2

Endogenous NA release enhances CA1 spike output via β-AR activation. (A) Schematic showing ex vivo slice recording and optogenetic stimulation. (B–D) Example traces (B), experiment timecourse (C) and grouped data (D) show 1 Hz tonic light stimulation (10 min, LED) to release endogenous NA enhances the spike probability in CA1 pyramidal neurons in response to Schaffer collateral synaptic stimulation (10 stimuli at 10 Hz) in slices from ChR2-injected but not WT mice. Scale bars = 25 mV, 250 ms. (E and F) Pre-incubation of slices with the β-AR antagonist, propranolol (500 nM) for 5 min prior to light stimulation blocked the increase in spike probability. Scale bars = 25 mV, 250 ms. (G and H) Phasic light stimulation (10 pulses at 25 Hz, immediately before synaptic stimuli) also increased spike probability but the increase was more variable. Scale bars = 25 mV, 250 ms.