Journal: Cell reports
Article Title: Sound-evoked adenosine release in cooperation with neuromodulatory circuits permits auditory cortical plasticity and perceptual learning
doi: 10.1016/j.celrep.2024.113758
Figure Lengend Snippet: (A and B) Schematics of electrical (A) or optogenetic (B) activation of the NB or VTA cell bodies. A bipolar stimulating electrode was inserted into the NB or VTA of WT mice (A), and an optical fiber was inserted into the ChR2-expressing NB or VTA of ChAT Cre or DAT Cre mice, respectively (B). (C and D) Mean normalized peak SEAR in the ACx measured in response to broadband noise (5 s) before, during, and after pairing with NB electrical stimulation (C, 5 black dots) or NB optical stimulation (D, 5 blue dots) in control (electrical: paired t test t 18 = 16.1, 2-tailed *p < 0.001 relative to baseline, 14 mice; optical: paired t test, t 6 = 11.1, 2-tailed *p < 0.001 relative to baseline, 6 mice) or in scopolamine-treated mice (electrical: paired t test, t 12 = 0.56, 2-tailed p = 0.59 relative to baseline, 10 mice; optical: paired t test, t 5 = 0.52, 2-tailed p = 0.63 relative to baseline, 4 mice). In optogenetic experiments (D), the NBs of ChAT Cre mice were injected with AAV-Ef1a-DIO-hChR2(E123T/T159C)-EYFP ( NB ChR2 mice). (E and F) Mean normalized peak SEAR in the ACx as a function of time measured before, during, and after pairing broadband noise with electrical (E, 5 black dots) or optical (F, 5 blue dots) stimulation of the VTA in control (electrical: paired t test, t 23 = 19.1, 2-tailed *p < 0.001 relative to baseline, 13 mice; optical: paired t test, t 6 = 7.4, 2-tailed *p < 0.001 relative to baseline, 5 mice), eticlopride-treated (electrical: paired t test, t 10 = 1.4, 2-tailed p = 0.19 relative to baseline, 7 mice; optical: paired t test, t 4 = 1.3, 2-tailed p = 0.29 relative to baseline, 3 mice), or SCH 23390-treated mice (electrical: Wilcoxon signed-rank test, W 8 = −36, *p = 0.008 relative to baseline, 6 mice). In optogenetic experiments (F), DAT Cre mice were injected into the VTA with AAV-Ef1a-DIO-hChR2(E123T/T159C)-EYFP ( VTA ChR2 mice). (G) Schematics of pairing an acoustic stimulus with electrical stimulation of the NB or VTA. (H and I) Normalized mean peak SEAR in ACx as a function of time delay between acoustic stimulus and NB (H) or VTA (I) stimulation in the respective pairing protocols (1-sample t test, Dt = 0.2 s, NB: t 4 = −6.6, 2-tailed *p = 0.003; VTA: t 4 = −12.4, 2-tailed *p < 0.001; Dt = −10 s and Dt = 10 s, p > 0.05, 5 mice each). Global fit curves (pseudo-Voigt approximation with 5 parameters) are also shown. (J) Representative SEAR in the ACx before, during, and after pairing broadband noise (5 s) with tail shock. (K) Mean normalized peak SEAR as a function of time before, during, and after paired (5 black dots, 300–400 ms between the tail shock and sound) or unpaired (5 red dots, 20 s between the tail shock and sound) delivery of tail shocks (5 dots) and broadband noise (5 s). Paired stimulation: paired t test, t 7 = 9.554, 2-tailed *p = 0.0003 relative to baseline, 8 mice. Unpaired stimulation: paired t test, t 2 = 3.9, 2-tailed p = 0.06 relative to baseline, 3 mice. Dashed line, baseline. Data are presented as the mean ± SEM.
Article Snippet: TC EPSCs were evoked by current pulses (100-μs duration) delivered to the thalamic radiation via tungsten bipolar electrodes (FHC, Inc.) placed in the white matter, midway between the MGv and the ACx (rostral to the hippocampus).
Techniques: Activation Assay, Expressing, Control, Injection
