ERK-dependent hyperexcitability of BLA neurons projecting to dCA3 underlies social dysfunction in a male mouse model of fragile X syndrome

BLA glutamatergic principal neurons nt-wprma5fcrr functionally connects to CA3 (Field CA3) MBA:463 · Mouse

After expressing ChR2 under the CaMKIIα promoter in BLA, blue light evoked EPSCs in dCA3 neurons recorded in slices; the responses persisted with TTX and 4-AP (monosynaptic) and were abolished by the AMPA receptor blocker DNQX, indicating a direct glutamatergic BLA-to-dCA3 connection.

Fig. 1J–L

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.

BLA (Basolateral amygdalar nucleus) MBA:295 synapses onto CA3 (Field CA3) MBA:463 · Mouse

Anterograde trans-synaptic AAV1-hSyn-Cre injected in the BLA together with a Cre-dependent GFP reporter in dorsal CA3 produced GFP-labelled neurons in dCA3, indicating BLA axons contact dCA3 neurons; labelling was comparable in Fmr1 KO and wild-type mice.

Fig. S3; Results, section 1 (anterograde trans-synaptic tagging)

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.

BLA (Basolateral amygdalar nucleus) MBA:295 projects to CA3 (Field CA3) MBA:463 · Mouse

Retrograde viruses (retroAAV-hSyn-mCherry or AAV11-hSyn-GFP) placed in dorsal CA3 labelled cell bodies in the BLA, showing that BLA neurons send axons to dCA3. The same retrograde strategy (retro-Cre in dCA3 with Cre-dependent GCaMP6m in BLA) was used for photometry of dCA3-projecting BLA neurons.

Fig. 1H–I; Fig. S3C–D; Results, section 1

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5) agrees.