Auditory input drives feed-forward inhibition onto LA interneurons, with cortical input producing a smaller E/I ratio than thalamic input¶

Claim · All claims
Evidence · 1 study · causal r2 · q3
Currency · newest study 2020 · not yet checked against its sources · not reviewed by a person

Subclaims¶

q3 i? AT or AC stimulation elicited biphasic responses (disynaptic inhibition, picrotoxin-sensitive) in about half of LA interneurons, and AC input drove feed-forward inhibition with a smaller E/I ratio than AT input (5.9 ± 1.1 vs 10.6 ± 1.9; p = 0.0453). → Polepalli 2020

Evidence¶

Polepalli 2020¶

Polepalli, J. S., Gooch, H. & Sah, P. (2020). Diversity of interneurons in the lateral and basal amygdala. npj Science of Learning 5:10. https://doi.org/10.1038/s41539-020-0071-z

q3 · i? · causal · r2

Slice electrophysiology with interneurons voltage-clamped at −40 mV; outward component blocked by the GABAA antagonist picrotoxin, indicating disynaptic inhibition in LA interneurons. "a smaller E/I ratio as compared to AT input"; only test statistics printed.

"We found that AC input drove feed-forward inhibition with a smaller E/I ratio as compared to AT input (AT-LA E/I ratio = 10.6 ± 1.9; AC-LA E/I ratio = 5.9 ± 1.1; p = 0.0453), consistent with the stronger AT input"

Discussion¶

Related Claims¶

• Thalamic input to accommodating (ACC) LA interneurons is significantly larger than cortical input to the same subtype — related
• Auditory thalamic and cortical input to BLA interneurons is concentrated in the LA: thalamic EPSCs are larger in LA than BA interneurons (191 vs 53 pA, p < 0.0001) — related
• Glutamatergic synapses on BA interneurons are less rectifying than those on LA interneurons, indicating fewer calcium-permeable GluR2-lacking AMPARs in the BA — related
• Long-term potentiation at cortical inputs is restricted to LA interneurons and cannot be induced in BA interneurons — related
• NMDAR subunit stoichiometry differs between LA and BA interneurons: LA NMDAR EPSCs decay faster and LA interneurons include a GluN2A-dominant majority plus NMDAR-lacking cells, absent in the BA
• Experimental work indicates basolateral amygdala cells activated by appetitive CSs mainly encode behavioural output, not CS identity, challenging amygdalo-centric feedforward accounts — related