Mouse
DR (Dorsal nucleus raphe) functionally connects to BLA (Basolateral amygdalar nucleus)
3 claims from 1 source: 3 found, 0 tested and absent, 0 ambiguous. Evidence: optogenetic circuit mapping.
The claims behind it
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.
DOI 10.1523/jneurosci.2238-16.2016 · PubMed 28087766 · PMC5320609, Fig. 2B,C; Results, 'Activation of 5-HT neurons evokes glutamate-mediated responses in BA INs'Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.
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.
DOI 10.1523/jneurosci.2238-16.2016 · PubMed 28087766 · PMC5320609, Fig. 3D–F; Fig. 4AMade by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.
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.
DOI 10.1523/jneurosci.2238-16.2016 · PubMed 28087766 · PMC5320609, Fig. 3A–C; Fig. 4AMade by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.