Loss of the Mecp2 gene in parvalbumin interneurons leads to an inhibitory deficit in the amygdala and affects its functional connectivity

BLA parvalbumin-expressing interneurons nt-fwck8mp6aj functionally connects to LA glutamatergic principal neurons nt-659aayyts5 · Mouse

After Cre-dependent ChR2 expression in parvalbumin interneurons of the basolateral amygdala, blue-light pulses evoked inhibitory postsynaptic currents in lateral amygdala principal neurons recorded with glutamate receptor blockers present; paired-pulse ratios differed between genotypes, indicating a lower GABA release probability when Mecp2 was deleted from the PV cells.

Fig. 1b; Results, section on PV output

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

LA (Lateral amygdalar nucleus) MBA:131 functionally connects to LA glutamatergic principal neurons nt-659aayyts5 · Mouse

Bursts of high-frequency electrical stimuli delivered at the cortical edge of the lateral amygdala, with AMPA, NMDA and GABA-A receptors blocked, produced a slow outward current in lateral amygdala principal neurons that was abolished by the GABA-B antagonist CGP 55845, showing local intra-LA interneuron input mediating slow inhibition; this response was smaller in mice lacking Mecp2 in PV cells.

Fig. 5a

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