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Excitability shifts in hippocampal circuitry point to pre-synaptic dysfunction after injury which is restored by application of <t>thalidomide.</t> (A-F) Fiber volley and fEPSP slope, at simulation ranging from 50 to 500 μA with error ellipses indicating 95% confidence. – demonstrate presynaptic dysfunctions, as the relationship between the fiber volley and the fEPSP does not significantly change after injury in all three subregions of the hippocampus. In – these disruptions are restored to sham levels post-thalidomide application in both area CA1 and omDG. However, in imDG , the correlation between fiber volley and fEPSP in injured vs. sham animals is different as shown by the lack of change in fiber volley slope and decreased overlap of the ellipses. This suggests that network excitability may be restored through a combination of presynaptic and postsynaptic means (see for details on analysis).
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Excitability shifts in hippocampal circuitry point to pre-synaptic dysfunction after injury which is restored by application of thalidomide. (A-F) Fiber volley and fEPSP slope, at simulation ranging from 50 to 500 μA with error ellipses indicating 95% confidence. – demonstrate presynaptic dysfunctions, as the relationship between the fiber volley and the fEPSP does not significantly change after injury in all three subregions of the hippocampus. In – these disruptions are restored to sham levels post-thalidomide application in both area CA1 and omDG. However, in imDG , the correlation between fiber volley and fEPSP in injured vs. sham animals is different as shown by the lack of change in fiber volley slope and decreased overlap of the ellipses. This suggests that network excitability may be restored through a combination of presynaptic and postsynaptic means (see for details on analysis).

Journal: Brain, behavior, and immunity

Article Title: Microglia depletion improves hippocampal circuit function after mild traumatic brain injury in male mice

doi: 10.1016/j.bbi.2025.106178

Figure Lengend Snippet: Excitability shifts in hippocampal circuitry point to pre-synaptic dysfunction after injury which is restored by application of thalidomide. (A-F) Fiber volley and fEPSP slope, at simulation ranging from 50 to 500 μA with error ellipses indicating 95% confidence. – demonstrate presynaptic dysfunctions, as the relationship between the fiber volley and the fEPSP does not significantly change after injury in all three subregions of the hippocampus. In – these disruptions are restored to sham levels post-thalidomide application in both area CA1 and omDG. However, in imDG , the correlation between fiber volley and fEPSP in injured vs. sham animals is different as shown by the lack of change in fiber volley slope and decreased overlap of the ellipses. This suggests that network excitability may be restored through a combination of presynaptic and postsynaptic means (see for details on analysis).

Article Snippet: Thalidomide (5 μM, Tocris Bioscience), an immunosuppressant ( ; ; ) was bath-applied in some slices from sham and injured animals to determine the effects of TNF-α on neural circuits.

Techniques:

Thalidomide restores excitability in hippocampal circuits at 7 dpi. (A) I/O curves of fEPSP slopes in area CA1 show no interaction effects; however, the significant increase in excitability in both injured and sham slices post 15-minute bath application of thalidomide suggest main effects of treatment; two-way ANOVA: F(1, 13) = 9.107, p < 0.0099. (B) Outer molecular layer Dentate Gyrus (omDG) show decreased excitability in injured slices after thalidomide application with no changes in sham slices; two-way ANOVA F(1, 117) = 18.23, p < 0.0001. (C) Inner molecular layer Dentate Gyrus (imDG) also revealed no changes in sham slices but an increase in excitability in injured animals post-thalidomide application; two-way ANOVA: F(1, 117) = 5.777, p = 0.0319. Data shown as mean ± SEM; Injured: N = 8; Sham: N = 7. Asterisks for multiple comparisons indicate ****p < 0.0001.

Journal: Brain, behavior, and immunity

Article Title: Microglia depletion improves hippocampal circuit function after mild traumatic brain injury in male mice

doi: 10.1016/j.bbi.2025.106178

Figure Lengend Snippet: Thalidomide restores excitability in hippocampal circuits at 7 dpi. (A) I/O curves of fEPSP slopes in area CA1 show no interaction effects; however, the significant increase in excitability in both injured and sham slices post 15-minute bath application of thalidomide suggest main effects of treatment; two-way ANOVA: F(1, 13) = 9.107, p < 0.0099. (B) Outer molecular layer Dentate Gyrus (omDG) show decreased excitability in injured slices after thalidomide application with no changes in sham slices; two-way ANOVA F(1, 117) = 18.23, p < 0.0001. (C) Inner molecular layer Dentate Gyrus (imDG) also revealed no changes in sham slices but an increase in excitability in injured animals post-thalidomide application; two-way ANOVA: F(1, 117) = 5.777, p = 0.0319. Data shown as mean ± SEM; Injured: N = 8; Sham: N = 7. Asterisks for multiple comparisons indicate ****p < 0.0001.

Article Snippet: Thalidomide (5 μM, Tocris Bioscience), an immunosuppressant ( ; ; ) was bath-applied in some slices from sham and injured animals to determine the effects of TNF-α on neural circuits.

Techniques: