Control of Amygdala Circuits by 5-HT Neurons via 5-HT and Glutamate Cotransmission

DR (Dorsal nucleus raphe) MBA:872 projects to BLA (Basolateral amygdalar nucleus) MBA:295 · Mouse

Cre-dependent AAV expressing ChR2-YFP injected into the dorsal raphe of SERT-Cre mice labelled axons throughout the basolateral amygdala, with the basal nucleus receiving a particularly dense plexus of YFP-positive, 5-HT-immunoreactive fibres; some of these varicosities also contained VGLUT3.

Fig. 1E–G; Results, 'Selective targeting of ChR2 expression to 5-HT neurons'

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DR (Dorsal nucleus raphe) MBA:872 functionally connects to BLA glutamatergic principal neurons nt-wprma5fcrr · Mouse

Thirty-second 20 Hz optical stimulation of raphe axons produced a slow outward current in nearly all basal amygdala principal neurons, reduced by the 5-HT1A antagonist WAY 100635 but not by GABA receptor blockers, and reduced the principal neurons' firing rate.

Fig. 5B–D,G

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DR (Dorsal nucleus raphe) MBA:872 functionally connects to BLA (Basolateral amygdalar nucleus) MBA:295 · Mouse

Single light pulses applied to ChR2-expressing raphe axons produced short-latency EPSCs in just over half of recorded basal amygdala interneurons; these currents were eliminated by combined AMPA/kainate and NMDA receptor blockade, showing glutamate release from 5-HT axons. The responses depressed as stimulation frequency rose from 1 to 20 Hz.

Fig. 2B,C; Results, 'Activation of 5-HT neurons evokes glutamate-mediated responses in BA INs'

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DR (Dorsal nucleus raphe) MBA:872 projects to LA (Lateral amygdalar nucleus) MBA:131 · Mouse

ChR2/YFP-labelled dorsal raphe axons also innervated the lateral amygdala, though the labelling there was less dense than in the adjacent basal nucleus.

Fig. 1E1,E2,F

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DR (Dorsal nucleus raphe) MBA:872 functionally connects to BLA glutamatergic principal neurons nt-wprma5fcrr · Mouse

Unlike interneurons, basal amygdala principal neurons showed no fast glutamatergic EPSC to single light pulses activating raphe axons, indicating that glutamate-releasing 5-HT terminals do not contact these cells.

Results, 'Activation of 5-HT neurons evokes 5-HT-mediated responses in BA PNs'; Fig. 5

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BLA (Basolateral amygdalar nucleus) MBA:295 functionally connects to BLA glutamatergic principal neurons nt-wprma5fcrr · Mouse

Optical activation of raphe axons at 20 Hz raised the frequency of spontaneous IPSCs in basal amygdala principal neurons; these events were abolished by GABA-A and GABA-B antagonists but not by a 5-HT1A antagonist, indicating a disynaptic GABAergic input from locally excited interneurons onto principal neurons.

Fig. 5E,F

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DR (Dorsal nucleus raphe) MBA:872 functionally connects to BLA (Basolateral amygdalar nucleus) MBA:295 · Mouse

High-frequency optical stimulation of raphe axons also produced a slow outward current in a subset of basal amygdala interneurons that was blocked by the 5-HT1A antagonist WAY 100635 and increased in amplitude with stimulation frequency.

Fig. 3D–F; Fig. 4A

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DR (Dorsal nucleus raphe) MBA:872 functionally connects to BLA (Basolateral amygdalar nucleus) MBA:295 · Mouse

With glutamate receptors blocked by kynurenic acid, 30 s trains of light at 20 Hz evoked a slow inward (excitatory) current in about half of basal amygdala interneurons, which was abolished by the 5-HT2A antagonist MDL 100907 and grew with increasing stimulation frequency.

Fig. 3A–C; Fig. 4A

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