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Hippocampal Theta Input to the Amygdala Shapes Feedforward Inhibition to Gate Heterosynaptic Plasticity.

Bazelot M, Bocchio M, Kasugai Y, Fischer D, Dodson PD, Ferraguti F, Capogna M - Neuron (2015)

Bottom Line: These effects are mediated by GABAB receptors and change in the Cl(-) driving force.Hence, feedforward inhibition, known to enforce temporal fidelity of excitatory inputs, dominates hippocampus-amygdala interactions to gate heterosynaptic plasticity.VIDEO ABSTRACT.

View Article: PubMed Central - PubMed

Affiliation: MRC Brain Network Dynamics Unit, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3TH, UK.

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Optical TBS of Hippocampal Axons Transiently Inhibits PNs and Triggers Firing in INs Ex vivo(A) Ex vivo cell-attached recording from a representative BA PN inhibited by TBS of vCA1 axons (ten superimposed sweeps, top; singularly represented in raster plot, bottom).(B) Pooled data showing PNs firing rates over time during TBS (bin = 50 ms, n = 7).(C) Firing rates of PNs compared between baseline, first, second, and tenth trains of the TBS. Firing is significantly reduced during the second train and partially recovers at tenth train.(D) Ex vivo cell-attached recording from a representative BA IN. TBS of vCA1 axons triggers action potentials (ten superimposed sweeps, top; singularly represented in raster plot, bottom).(E) Pooled data showing INs firing rates over time during TBS (bin = 50 ms, n = 7).(F) Firing rates of INs compared between baseline, first, second, and tenth trains of the TBS. Firing is significantly increased during TBS trains. ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001. Data are presented as means ± SEM.
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fig4: Optical TBS of Hippocampal Axons Transiently Inhibits PNs and Triggers Firing in INs Ex vivo(A) Ex vivo cell-attached recording from a representative BA PN inhibited by TBS of vCA1 axons (ten superimposed sweeps, top; singularly represented in raster plot, bottom).(B) Pooled data showing PNs firing rates over time during TBS (bin = 50 ms, n = 7).(C) Firing rates of PNs compared between baseline, first, second, and tenth trains of the TBS. Firing is significantly reduced during the second train and partially recovers at tenth train.(D) Ex vivo cell-attached recording from a representative BA IN. TBS of vCA1 axons triggers action potentials (ten superimposed sweeps, top; singularly represented in raster plot, bottom).(E) Pooled data showing INs firing rates over time during TBS (bin = 50 ms, n = 7).(F) Firing rates of INs compared between baseline, first, second, and tenth trains of the TBS. Firing is significantly increased during TBS trains. ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001. Data are presented as means ± SEM.

Mentions: Next, we wished to test whether TBS-evoked inhibition of PNs spontaneous firing occurred in a slice preparation. In these conditions, long-range projections to the BA are cut, ruling out that their stimulation would in turn trigger activation of other regions projecting to the BA. First, we optically activated vCA1 fibers at theta frequency while recording from BA neurons in cell-attached mode, using light intensities sufficient to evoke an action potential in INs but not in PNs (range: 2 to 3 mW/mm2). Optogenetic TBS transiently inhibited the firing of PNs (Figures 4A–4C, second train versus baseline p < 0.0001, n = 7). In contrast, TBS triggered action potentials synchronized to each light train in INs (Figures 4D–4F, second train versus baseline p < 0.01, n = 7). We also used higher light intensities, sufficient to evoke action potentials in PNs (>10 mW/mm2) to examine the impact of TBS on evoked firing. In this case, optogenetic TBS transiently depressed the evoked spike probability in BA PNs (Figures S6A and S6B, second versus first TBS trains p < 0.001, n = 22) via activation of GABAB receptors (Figures S6E and S6F, second versus first train p > 0.05, n = 9). In contrast, TBS did not reduce the spike probability of INs (Figures S6C and S6D, second versus first TBS trains p > 0.05, n = 10). These results suggest that the activation of hippocampal fibers at theta frequency preferentially recruits GABAergic INs of the BA, inhibiting the spontaneous firing of PNs or sculpting their hippocampal-driven firing via FFI.


Hippocampal Theta Input to the Amygdala Shapes Feedforward Inhibition to Gate Heterosynaptic Plasticity.

Bazelot M, Bocchio M, Kasugai Y, Fischer D, Dodson PD, Ferraguti F, Capogna M - Neuron (2015)

Optical TBS of Hippocampal Axons Transiently Inhibits PNs and Triggers Firing in INs Ex vivo(A) Ex vivo cell-attached recording from a representative BA PN inhibited by TBS of vCA1 axons (ten superimposed sweeps, top; singularly represented in raster plot, bottom).(B) Pooled data showing PNs firing rates over time during TBS (bin = 50 ms, n = 7).(C) Firing rates of PNs compared between baseline, first, second, and tenth trains of the TBS. Firing is significantly reduced during the second train and partially recovers at tenth train.(D) Ex vivo cell-attached recording from a representative BA IN. TBS of vCA1 axons triggers action potentials (ten superimposed sweeps, top; singularly represented in raster plot, bottom).(E) Pooled data showing INs firing rates over time during TBS (bin = 50 ms, n = 7).(F) Firing rates of INs compared between baseline, first, second, and tenth trains of the TBS. Firing is significantly increased during TBS trains. ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001. Data are presented as means ± SEM.
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Related In: Results  -  Collection

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fig4: Optical TBS of Hippocampal Axons Transiently Inhibits PNs and Triggers Firing in INs Ex vivo(A) Ex vivo cell-attached recording from a representative BA PN inhibited by TBS of vCA1 axons (ten superimposed sweeps, top; singularly represented in raster plot, bottom).(B) Pooled data showing PNs firing rates over time during TBS (bin = 50 ms, n = 7).(C) Firing rates of PNs compared between baseline, first, second, and tenth trains of the TBS. Firing is significantly reduced during the second train and partially recovers at tenth train.(D) Ex vivo cell-attached recording from a representative BA IN. TBS of vCA1 axons triggers action potentials (ten superimposed sweeps, top; singularly represented in raster plot, bottom).(E) Pooled data showing INs firing rates over time during TBS (bin = 50 ms, n = 7).(F) Firing rates of INs compared between baseline, first, second, and tenth trains of the TBS. Firing is significantly increased during TBS trains. ∗∗p < 0.01; ∗∗∗p < 0.001; ∗∗∗∗p < 0.0001. Data are presented as means ± SEM.
Mentions: Next, we wished to test whether TBS-evoked inhibition of PNs spontaneous firing occurred in a slice preparation. In these conditions, long-range projections to the BA are cut, ruling out that their stimulation would in turn trigger activation of other regions projecting to the BA. First, we optically activated vCA1 fibers at theta frequency while recording from BA neurons in cell-attached mode, using light intensities sufficient to evoke an action potential in INs but not in PNs (range: 2 to 3 mW/mm2). Optogenetic TBS transiently inhibited the firing of PNs (Figures 4A–4C, second train versus baseline p < 0.0001, n = 7). In contrast, TBS triggered action potentials synchronized to each light train in INs (Figures 4D–4F, second train versus baseline p < 0.01, n = 7). We also used higher light intensities, sufficient to evoke action potentials in PNs (>10 mW/mm2) to examine the impact of TBS on evoked firing. In this case, optogenetic TBS transiently depressed the evoked spike probability in BA PNs (Figures S6A and S6B, second versus first TBS trains p < 0.001, n = 22) via activation of GABAB receptors (Figures S6E and S6F, second versus first train p > 0.05, n = 9). In contrast, TBS did not reduce the spike probability of INs (Figures S6C and S6D, second versus first TBS trains p > 0.05, n = 10). These results suggest that the activation of hippocampal fibers at theta frequency preferentially recruits GABAergic INs of the BA, inhibiting the spontaneous firing of PNs or sculpting their hippocampal-driven firing via FFI.

Bottom Line: These effects are mediated by GABAB receptors and change in the Cl(-) driving force.Hence, feedforward inhibition, known to enforce temporal fidelity of excitatory inputs, dominates hippocampus-amygdala interactions to gate heterosynaptic plasticity.VIDEO ABSTRACT.

View Article: PubMed Central - PubMed

Affiliation: MRC Brain Network Dynamics Unit, Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3TH, UK.

Show MeSH