Journal: The Journal of Neuroscience

Article Title: A Role for Thalamic Projection GABAergic Neurons in Circadian Responses to Light

doi: 10.1523/JNEUROSCI.0112-21.2022

Figure Lengend Snippet: Ablation of Sox14 + IGL/LGv neurons causes delayed vigilance state transitions at circadian light changes. A , B , Spectrograms, EEG/EMG traces, and hypnograms over a 1-h period from a representative control mouse and an ablated mouse. C , Over a 24-h period, control and Sox14 + IGL/LGv-ablated mice spend a similar percentage of time in Wake (48.24 ± 1.96% vs 48.22 ± 1.71%, p = 0.99), NREM (46.73 ± 1.80% vs 46.38 ± 1.71%, p = 0.89), and REM (5.03 ± 0.20% vs 5.39 ± 0.17%, p = 0.2). Values are mean ± SEM, t test. D , E , Distribution of Wake, NREM, and REM in the 2 h preceding and following each light transition. Light and dark hours are shaded in yellow and gray, respectively (see Extended Data for comprehensive statistics). F , Pairwise comparison in the content of Wake, NREM, and REM between the hour preceding and each of the 2 h following the light to dark transition. Control group: Wake −1 : 33.17 ± 2.98%, Wake 1 : 80.26 ± 3.49%, p < 0.0001, Wake 2 : 72.61 ± 7.76%, p = 0.001; NREM −1 : 60.08 ± 2.65%, NREM 1 : 18.39 ± 3.29%, p = 0.0001, NREM 2 : 25.17 ± 7.04%, p = 0.0015; REM -1 : 6.75 ± 0.52%, REM 1 : 1.35 ± 0.45% p = 0.0004, REM 2 : 2.18 ± 0.85% p = 0.007. Ablated group: Wake −1 36.57 ± 5.34%, Wake 1 : 56.67 ± 3.49%, p = 0.093, Wake 2 : 75.23 ± 7.24%, p = 0.008; NREM −1 56.35 ± 4.73%, NREM 1 : 38.19 ± 7.68%, p = 0.093, NREM 2 : 22.36 ± 6.64%, p = 0.0081; REM -1 : 7.08 ± 0.78%, REM 1 : 5.10 ± 1.16%, p = 0.296, REM 2 : 2.41 ± 0.90%, p = 0.031. Values are mean ± SEM, t test except Control REM -1 versus REM 2 , Ablated REM -1 versus REM 1 and REM 2 Wilcoxon test. G , Pairwise comparison in the content of Wake, NREM, and REM between the hour preceding and each of the 2 h following the dark to light transition. Control group: Wake −1 : 94.77 ± 3.48%, Wake 1 : 63.47 ± 9.42%, p = 0.015, Wake 2 : 36.11 ± 9.72%, p = 0.015; NREM −1 : 5.22 ± 3.48%, NREM 1 : 34.87 ± 8.82% p = 0.015, NREM 2 : 57.51 ± 8.86% p = 0.015; REM -1 : 0.00 ± 0.00%, REM 1 : 1.66 ± 0.64%, p = 0.125, REM 2 : 6.37 ± 1.09%, p = 0.015. Ablated group: Wake −1 79.18 ± 7.51%, Wake 1 : 82.47 ± 7.80%, p = 0.812, Wake 2 : 39.37 ± 8.09%, p = 0.017; NREM −1 20.50 ± 7.34%, NREM 1 : 17.25 ± 7.65%, p = 0.848, NREM 2 : 56.31 ± 7.22%, p = 0.021; REM -1 : 0.31 ± 0.21%, REM 1 : 0.27 ± 0.20%, p > 0.999, REM 2 : 4.31 ± 1.34%, p = 0.0313. Values are mean ± SEM, Wilcoxon test except Ablated Wake −1 versus Wake 2 and NREM −1 versus NREM 2 t test. H , Fold change in distance traveled in the light phase (12 h). Total distance in the dark phase (12 h) was set at 1. Control group: 1.0 ± 0.14 (dark) versus 0.77 ± 0.26 (light); Ablated group: 1.0 ± 0.17 (dark) versus 0.52 ± 0.82 (light). I , Example trajectories for one control and one ablated mouse in the hour preceding and following the light change. Oval: ROI used for automated tracking; yellow: light, gray: dark. Histograms report the fold change in distance traveled in the hour preceding and following the light change. For the light to dark transition distance in the light was set at 1: Control group 1.0 ± 0.21 (light) 5.59 ± 1.36 (dark), p = 0.0078; Ablated group 1.0 ± 0.17 (light) 2.80 ± 0.68 (dark), p = 0.044. J , For the dark to light transition distance in the dark was set at 1: Control group 1.0 ± 0.15 versus 0.64 ± 0.31, p = 0.148; Ablated group 1.0 ± 0.28 versus 0.92 ± 0.29, p = 0.468. Values are mean ± SEM, Wilcoxon test except for Ablated light to dark transition t test. N.s.: not statistically significant. A summary of statistical tests is available in Extended Data .

Article Snippet: The EEG/EMG signals were sampled at 250 Hz, amplified 100×, and low-pass filtered at 100 Hz using a two EEG channel, two EMG channel mouse preamplifier (Pinnacle Technology Inc).

Techniques: Control, Comparison

Journal: Neuroscience

Article Title: Post-ictal generalized EEG suppression is reduced by enhancing dorsal raphe serotonergic neurotransmission

doi: 10.1016/j.neuroscience.2020.11.029

Figure Lengend Snippet: PGES was consistently observed following seizures in amygdala kindled mice. (A) Top: 500 s raw EEG trace depicting seizure stimulation (Stim), seizure (Sz), PGES (duration indicated by horizontal line), and gradual EEG recovery in a C57BL/6J mouse. Scale bars: horizontal, 50 s; vertical, 2 μV. Bottom traces correspond to boxes on top trace and demonstrate EEG at baseline and during PGES. Scale bars: horizontal, 5 s; vertical 2 μV. (B) Nissl stained coronal hemi-section demonstrating electrode tract (arrowheads) in the basolateral amygdala. HPC, hippocampus; 3V, third ventricle; BLA, basolateral amygdala. Scale bar: 3 mm. (C) 150 s raw EEG (top), EMG (middle), and plethysmography (Pleth; bottom) traces depicting a spontaneous seizure (highlighted) emerging from non-rapid eye movement (NREM) in a kindled mouse. PGES duration is indicated by horizontal line. Scale bars: horizontal, 10 s; vertical 2 μV. (D) 150 s raw EEG (top), EMG (middle), and plethysmography (bottom) traces depicting a seizure stimulation and seizure (highlighted) that led to death in a kindled mouse. Scale bars: horizontal, 10 s; vertical 2 μV. *, Artifact from opening chamber. (E,F) Average seizure durations (E) and PGES durations (F) in the amygdala kindled mice. (G) Linear regression analysis of seizure duration in amygdala kindled mice versus PGES duration. Symbols represent different groups of animals.

Article Snippet: An EEG/EMG preamplifier (8202-SL; Pinnacle Technology; Lawrence, KS) and a 3-channel electrode cable (335–340/3; Plastics One) were attached to the animal’s headmount and connected to a data conditioning amplifier (LP511AC; AstroNova; West Warwick, RI), a stimulating/recording switch (SRS-13C0113G; AstroNova), and a pulse stimulator (Model 2100; A-M Systems).

Techniques: Staining