4 research outputs found
Differential effects of total sleep deprivation on contextual and spatial memory: Modulatory effects of modafinil
Low β2 Main Peak Frequency in the Electroencephalogram Signs Vulnerability to Depression
International audienceObjective: After an intense and repeated stress some rats become vulnerable to depression. This state is characterized by persistent low serum BDNF concentration. Our objective was to determine whether electrophysiological markers can sign vulnerability to depression.Methods: Forty-three Sprague Dawley rats were recorded with supradural electrodes above hippocampus and connected to wireless EEG transmitters. Twenty-nine animals experienced four daily social defeats (SD) followed by 1 month recovery. After SD, 14 rats had persistent low serum BDNF level and were considered as vulnerable (V) while the 15 others were considered as non-vulnerable (NV). EEG signals were analyzed during active waking before SD (Baseline), just after SD (Post-Stress) and 1 month after SD (Recovery).Results: We found that V animals are characterized by higher high θ and α spectral relative powers and lower β2 main peak frequency before SD. These differences are maintained at Post-Stress and Recovery for α spectral relative powers and β2 main peak frequency. Using ROC analysis, we show that low β2 main peak frequency assessed during Baseline is a good predictor of the future state of vulnerability to depression.Conclusion: Given the straightforwardness of EEG recordings, these results open the way to prospective studies in humans aiming to identify population at-risk for depression
Low β2 Main Peak Frequency in the Electroencephalogram Signs Vulnerability To Depression.
Objective:After an intense and repeated stress some rats become vulnerable to depression. This state is characterized by persistent low serum BDNF concentration. Our objective was to determine whether electrophysiological markers can sign vulnerability to depression. Methods:Forty-three Sprague Dawley rats were recorded with supradural electrodes above hippocampus and connected to wireless EEG transmitters. Twenty-nine animals experienced four daily social defeats (SD) followed by one month recovery. After SD, 14 rats had persistent low serum BDNF level and were considered as vulnerable (V) while the 15 others were considered as non-vulnerable (NV). EEG signals were analyzed during active waking before SD (Baseline), just after SD (Post-Stress) and 1 month after SD (Recovery).Results:We found that V animals are characterized by higher high θ and α spectral relative powers and lower β2 main peak frequency before SD. These differences are maintained at Post-Stress and Recovery for α spectral relative powers and β2 main peak frequency. Using ROC analysis, we show that low β2 main peak frequency assessed during Baseline is a good predictor of the future state of vulnerability to depression.Conclusion:Given the straightforwardness of EEG recordings, these results open the way to prospective studies in humans aiming to identify population at-risk for depression
Interaction between diazepam and hippocampal corticosterone after acute stress: impact on memory in middle-aged mice
Benzodiazepines (BDZ) are widely prescribed in the treatment of anxiety disorders associated to aging. Interestingly, whereas a reciprocal interaction between the GABAergic system and HPA axis has been evidenced, there is to our knowledge no direct evaluation of the impact of BDZ on both hippocampus (HPC) corticosterone concentrations and HPC-dependent memory in stressed middle-aged subjects. We showed previously that an acute stress induced in middle-aged mice severe memory impairments in a hippocampus-dependent task, and increased in parallel hippocampus corticosterone concentrations, as compared to non stressed middle-aged controls (Tronche et al., 2010). Based on these findings, the aims of the present study were to evidence the impact of diazepam (a positive allosteric modulator of the GABA-A receptor) on HPC glucocorticoids concentrations and in parallel on HPC-dependent memory in acutely stressed middle-aged mice.Microdialysis experiments showed an interaction between diazepam doses and corticosterone concentrations into the HPC. From 0.25 mg/kg to 0.5 mg/kg, diazepam dose-dependently reduces intra-HPC corticosterone concentrations and in parallel, dose-dependently increased hippocampal-dependent memory performance. In contrast, the highest (1.0mg/kg) diazepam dose induces a reduction in HPC corticosterone concentration, which was of greater magnitude as compared to the two other diazepam doses, but however decreased the hippocampal-dependent memory performance. In summary, our study provides first evidence that diazepam restores in stressed middle-aged animals the hippocampus-dependent response, in relation with HPC corticosterone concentrations. Overall, our data illustrate how stress and benzodiazepines could modulate cognitive functions depending on hippocampus activity
