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. 2022 Oct 19;42(42):7921–7930. doi: 10.1523/JNEUROSCI.2032-21.2022

Figure 6.

Figure 6.

DE does not alter the strength of corticothalamic feedback excitatory synaptic transmission from V1 L6 to TRN. A, Circuit diagram highlighting V1 input to TRN. B, Confocal image of a horizontal brain slice of an Ntsr1-Cre (L6-Cre) mouse injected with AAV-dflox-ChR2-EYFP (green) in V1 L6. The section is counterstained with DAPI (blue). Note ChR2-EYFP-expressing axons in TRN. Left, Lower magnification showing ChR2-EYFP-expressing axons in TRN. LGv, Ventral lateral geniculate nucleus; HC, hippocampus. Right, Higher magnification of TRN. Bright small puncta correspond to boutons. Cell bodies visibly lack EYFP signals. C, ChR2-evoked Sr2+-mEPSCs recorded from TRN neurons. Left, Example traces from NR and DE mice. A 5 ms LED pulse duration was used. Labels are the same as in Figure 1D. Middle, Comparison of the average amplitude of ChR2-evoked Sr2+-mEPSCs (NR: 25.0 ± 2.9 pA, 16 cells from 8 mice; DE: 25.5 ± 2.9 pA, 12 cells from 5 mice; t test: t(26) = 0.1039, p = 0.918). Note that spontaneous mEPSCs recorded from TRN neurons (16 NR cells) display fast kinetics (decay tau = 1.92 ± 0.31 ms, 10–90% rise time = 0.57 ± 0.08 ms) and high frequency (19.1 ± 0.3 Hz) typical of PV-positive inhibitory neurons. Bars, Mean ± SEM; gray circles, average value for each cell. Right, Average ChR2-evoked Sr2+-mEPSC traces from NR and DE.