Article Figures & Data
Figures
- Figure 1.
The 10 Hz mPFC stimulation has opposite effects on aBNST plasticity in control and stressed anesthetized mice. A, Time line of experiment. B, Stimulation and recording protocol. C, Histological controls of stimulation (mPFC, lesion at arrow) and recording (aBNST, blue spot at arrow) sites. Scale bar, 1 mm. D, E, Graphs illustrating the effects of stress on basal activity frequency (D) and cortical excitation strength (E). F, Kinetic (left) and quantification (right) of the mean percentage change (±SEM) in mPFC-evoked spike probability, normalized to the baseline, after 10 Hz mPFC stimulation (at t0) in control and stressed mice. G, Typical PSTHs and associated rasters illustrate responses of aBNST neurons before and after 10 Hz mPFC stimulation in control (left) and stressed mice (right). Stimulus at t0 (gray lines). Bin width, 1 ms. Representative electrophysiological traces in insets. H, Quantification of basal firing activity of aBNST neurons (mean ± SEM) before and 35–40 min after 10 Hz mPFC stimulation in control and stressed mice. I, Time line of experiment. J, Kinetic (left) and quantification (right) of the mean percentage change (±SEM) in mPFC-evoked spike probability, normalized to the baseline, after 10 Hz mPFC stimulation (at t0) in stressed mice pretreated with RU486 or vehicle. N = number of mice; n = number of neurons. *indicates significant differences between control and stress groups; + indicates significant differences between baseline (before) and 35–40 min after 10 Hz mPFC stimulation. +p < 0.05, **p < 0.01; ***p < 0.001. Numbers in brackets of histogram bars refer to the number of aBNST neurons recorded. The same nomenclature is used for all figure legends.
- Figure 2.
CB1+/+ and CB1−/− mice displayed a similar response to stress. A–F, Effect of acute stress on Fos-immunoreactive neurons in PVN, mPFC, and aBNST of control and stressed CB1+/+ or CB1−/− mice. A, C, E, Histograms showing the density of Fos-positive neurons after an acute stress in CB1+/+ and CB1−/− mice. PVN and mPFC displayed the expected enhancement of stress-induced cellular activation in CB1+/+ but also in CB1−/− mice. Stress-induced Fos staining was similar in CB1+/+ and CB1−/− mice. B, D, F, Representative micrographs of immunostained sections for Fos of the PVN (B), mPFC (D), and aBNST (F). Note that no stress-induced Fos activation was observed in the aBNST of CB1+/+ or CB1−/− mice (E, F). + indicates significant differences between control and stress groups. +p < 0.05, ++p < 0.01. Scale bars: B, 0.4 mm; D, 0.2 mm; F, 0.6 mm. ac, Anterior commissure; PL, prelimbic cortex; IL, infralimbic cortex; cc, corpus callosum; Ov, oval nucleus; aBNSTv, ventral part of aBNST; dBNSTd, dorsal part of aBNST; 3V, third ventricle. Numbers in brackets of histogram bars refer to the number of mice used.
- Figure 3.
Neuroplastic changes in the aBNST depend on CB1-Rs activation. A, B, Kinetic (left) and quantification (right) of the mean percentage change (±SEM) in mPFC-evoked spike probability, normalized to the baseline, after 10 Hz mPFC stimulation (at t0) in control and stressed CB1+/+ or CB1−/− mice. C–F, Graphs illustrating the effects of stress and/or 10 Hz mPFC stimulation on basal activity frequency (C, E, F) and cortical excitation strength (D). See Figure 1 legend for nomenclature.
- Figure 4.
CB1-Rs that control LTD and LTP are located in the aBNST on mPFC terminals. A, Stimulation and recording protocol. B, The CB1-R antagonist AM251 (60 nl, 1 μm) or vehicle was infused into the aBNST before 10 Hz mPFC stimulation in stressed mice. Kinetic (left) and quantification (right) of the mean percentage change (±SEM) in mPFC-evoked spike probability, normalized to the baseline, after 10 Hz mPFC stimulation (at t0) after vehicle (VEH) or AM251 infusion in the aBNST of stressed mice. C, D, Kinetic (left) and quantification (right) of the mean percentage change (±SEM) in mPFC-evoked spike probability, normalized to the baseline, after 10 Hz mPFC stimulation (at t0) in control and stressed Glu-CB1+/+(C) or Glu-CB1−/−(D) mice. See Figure 1 legend for nomenclature.
