BLA (Basolateral amygdalar nucleus) functionally connects to CA1 (Field CA1)

Activating ChR2 confined to GABAergic BA neurons evoked inhibitory (inward, high-chloride internal) currents in roughly half of the identified vH interneurons recorded, showing that the long-range inhibitory projection also targets local interneurons.

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Paired recordings of NAc-projecting and BA-projecting vH neurons in the same field of view showed that light-evoked excitatory BA input was on average equal onto the two populations (9 pairs with pan-neuronal ChR2; 10 pairs with CaMKii ChR2).

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In 7 pairs of PFC-projecting and BA-projecting vH neurons, activation of GABAergic BA axons produced essentially no inhibitory current in the PFC-projecting cells.

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Light activation of basal amygdala axons expressing ChR2 under the synapsin promoter evoked short-latency currents at -70 mV in about 40% of recorded ventral hippocampal pyramidal neurons, and these currents were abolished by the AMPA receptor blocker NBQX (n = 9 neurons).

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Paired recordings showed that long-range inhibitory BA input reached NAc-projecting vH neurons, but with consistently smaller amplitude than in neighbouring BA-projecting neurons (7 pairs); the authors describe this as a weak connection.

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With ChR2 restricted to excitatory basal amygdala neurons by the CaMKii promoter, light evoked large currents at 0 mV in vH pyramidal cells that were completely abolished by NBQX, showing the inhibition was purely disynaptic feedforward inhibition driven by a glutamatergic BA input (n = 3 neurons).

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5-5) disagrees. “Fig 2F,G records NBQX-sensitive inhibitory currents at 0 mV, so it does not show a direct excitatory connection onto pyramidal cells; the sign is wrong for this evidence.”

In 8 pairs of neighbouring PFC-projecting and BA-projecting vH neurons, light activation of pan-neuronal BA input produced essentially no excitatory current in the PFC-projecting cells while the BA-projecting partner responded.

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Recording from fluorescently identified vGAT+ interneurons in ventral hippocampus, light activation of BA axons evoked excitatory currents at -70 mV in about half of the interneurons tested.

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Light stimulation of basal amygdala axons expressing ChR2 pan-neuronally evoked currents at 0 mV in roughly 30% of vH pyramidal neurons that were blocked by gabazine. In 4 of 12 cells with inhibitory responses part of the current survived NBQX, indicating direct long-range inhibition in addition to feedforward inhibition.

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With cre-dependent ChR2 in GABAergic BA neurons, light-evoked inhibitory currents were consistently larger in BA-projecting vH neurons than in neighbouring NAc-projecting (7 pairs) or PFC-projecting (7 pairs) neurons.

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With cre-dependent ChR2 confined to GABAergic basal amygdala neurons in vGAT-cre mice, light evoked robust currents at 0 mV in vH pyramidal neurons that were insensitive to NBQX but blocked by gabazine, demonstrating a direct long-range inhibitory connection (n = 6 neurons).

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In paired recordings of neighbouring retrogradely labelled vH neurons, light activation of pan-neuronal (and separately CaMKii-restricted) BA axons evoked excitatory currents at -70 mV in BA-projecting vH neurons; these were equal to those in neighbouring NAc-projecting cells and much larger than in PFC-projecting cells.

Made by an AI model reading the paper (claude-opus-5, extract@0.3.0); a second AI model (claude-opus-5-5) disagrees. “The paper reports no connection probability of 1.0 for vHBA cells; the paired designs used 9, 8 and 10 pairs, so this number is unsupported.”