Mouse
PL (Prelimbic area) functionally connects to BLA glutamatergic principal neurons
5 claims from 5 sources: 5 found, 0 tested and absent, 0 ambiguous. Evidence: electrical stimulation, optogenetic circuit mapping.
The claims behind it
Light activation of ChR2-expressing dorsomedial prefrontal axons in slices produced biphasic currents in basolateral amygdala principal neurons: a short-latency monosynaptic EPSC (about 4 ms onset, abolished by TTX and partly restored with 4-AP) followed by a longer-latency disynaptic IPSC that was blocked by glutamate receptor antagonists or by picrotoxin, indicating feedforward recruitment of local interneurons.
DOI 10.1038/s41467-020-15920-7 · PubMed 32376858 · PMC7203160, Fig. 1d–h; Supplementary Fig. 1a–fMade by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.
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.
DOI 10.1016/j.isci.2026.114753 · PubMed 41684844 · PMC12890714, Fig. 6A–6GMade by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.
Blue-light activation of ChR2-expressing dmPFC terminals in the basal amygdala evoked monosynaptic AMPA- and NMDA-receptor-mediated EPSCs in BA principal neurons recorded in whole-cell mode; EPSCs persisted with GABA-A blockade by bicuculline, and paired-pulse ratio, input-output and AMPA/NMDA ratio were measured at this synapse.
DOI 10.1038/s41398-020-00926-y · PubMed 32684634 · PMC7370229, Figs. 1a, d–i; 2a–c; 3a–cMade by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.
About 85% of the Fos-positive nuclei driven in the medial basolateral amygdala by prefrontal D1 photostimulation were CaMKII-positive (roughly 20% of CaMKII cells in this territory). Silencing these CaMKII neurons with halorhodopsin and yellow light abolished the feeding increase produced by blue-light stimulation of the prefrontal D1 terminals, indicating that the prefrontal input acts through these amygdala glutamatergic cells.
DOI 10.1038/nn.3625 · PubMed 24441680 · PMC3968853, Fig. 5d,f; Fig. 6g-iMade by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.
In slices where the PL-to-BLA pathway was preserved, BLA pyramidal neurons of sgTmem74 mice fired more action potentials; this hyperexcitability disappeared in slices in which the PL-BLA connection was severed, implying functional excitatory drive from PL onto BLA pyramidal neurons.
DOI 10.1038/s41380-023-01954-y · PubMed 36690791 · PMC10611563, Supplementary Fig. 5d–jMade by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) disagrees. “The evidence was slice preparation preserving versus severing the pathway with whole-cell recording, not electrical stimulation.”