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PL (Prelimbic area) functionally connects to BLA glutamatergic principal neurons
All claims for this connection- Species
- Mouse
- Result
- present
- Method
- optogenetic circuit mapping
- Sign
- excitatory
- Evidence
- Optogenetic activation of PrL glutamatergic axon terminals in the BLA lowered mechanical thresholds in control mice, and this effect was abolished when BLA glutamatergic neurons were chemogenetically silenced; conversely, silencing PrL terminals in BLA raised thresholds in tumour-bearing mice and this was reversed by chemogenetic excitation of BLA glutamatergic neurons. A glutamate sensor in the BLA showed that chemogenetic inhibition of PrL VGluT2+ neurons reduced evoked glutamate release in the BLA, indicating an excitatory PrL-to-BLA functional connection.
- Source
Prelimbic cortex-basolateral amygdala glutamatergic circuit drives cancer-induced bone pain in mice
iScience, 2026
DOI 10.1016/j.isci.2026.114753 · PubMed 41684844 · PMC12890714, Fig. 6A–6GLicence: CC-BY-NC-4.0
- Named in the paper
- “PrLGlu” and “BLAGlu neurons”
- Made by
- an AI model reading the paper (claude-opus-5, extract@0.3.0), 2026-10-09
- Checked by
a second AI model (claude-opus-5) agrees, 2026-10-09
“Combined opto-terminal stimulation/silencing with opposing chemogenetic manipulation of BLA Glu neurons plus the glutamate sensor data support an excitatory functional PrL→BLA connection, though the Fig. 6F/G wording is internally inconsistent.”
- Status
proposed
Drafted and checked by AI models; it stays proposed until people have audited a sample of such claims.