Hippocampal Theta Input to the Amygdala Shapes Feedforward Inhibition to Gate Heterosynaptic Plasticity

CA1 (Field CA1) MBA:382 projects to CEA (Central amygdalar nucleus) MBA:536 · Mouse

Few ChR2-YFP-labelled hippocampal fibres were detectable in the central amygdala.

Fig. 2B legend

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

CA1 (Field CA1) MBA:382 projects to BLA (Basolateral amygdalar nucleus) MBA:295 · Mouse

After Cre-dependent ChR2-YFP expression in ventral/intermediate CA1 pyramidal cells, labelled axons innervated the basal amygdala densely.

Fig. 2B

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

LA (Lateral amygdalar nucleus) MBA:131 functionally connects to BLA glutamatergic principal neurons nt-wprma5fcrr · Mouse

Electrical stimulation of the lateral amygdala evoked monosynaptic EPSPs in BA principal neurons. These EPSPs were potentiated long-term only when LA theta burst stimulation was paired 10 ms after optical theta burst stimulation of vCA1 axons.

Fig. 8A-D; Fig. S8A-B

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

CA1 (Field CA1) MBA:382 synapses onto BLA glutamatergic principal neurons nt-wprma5fcrr · Mouse

Electron microscopy showed that ChR2-YFP-labelled ventral CA1 axons formed synapses on dendrites of basal amygdala principal neurons, preferentially on spines according to confocal analysis.

Figs. S3C, S3D; Results

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

CA1 (Field CA1) MBA:382 functionally connects to BLA (Basolateral amygdalar nucleus) MBA:295 · Mouse

Photostimulation of ventral CA1 axons evoked monophasic EPSPs in BA interneurons (pooled with intercalated cells), and it evoked spiking at lower light power than in principal neurons. Theta burst stimulation increased interneuron firing both in vivo and ex vivo.

Figs. 2F-G, 3D-F, 4D-F, 5F

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

CA1 (Field CA1) MBA:382 projects to BMA (Basomedial amygdalar nucleus) MBA:319 · Mouse

ChR2-YFP-labelled axons from ventral CA1 densely innervated the basomedial nucleus, along with the BA.

Fig. 2B

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

CA1 (Field CA1) MBA:382 synapses onto BLA (Basolateral amygdalar nucleus) MBA:295 · Mouse

Electron microscopy confirmed that ventral CA1 axons formed synapses on dendrites of basal amygdala GABAergic interneurons, mostly on dendritic shafts.

Figs. S3C, S3D; Results

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

BLA (Basolateral amygdalar nucleus) MBA:295 functionally connects to BLA glutamatergic principal neurons nt-wprma5fcrr · Mouse

Local electrical stimulation under NBQX/APV evoked monosynaptic IPSPs and IPSCs in BA principal neurons. Baclofen abolished these responses, and their paired-pulse ratio depended on the inter-stimulus interval.

Fig. 7A-C

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

CA1 (Field CA1) MBA:382 functionally connects to BLA glutamatergic principal neurons nt-wprma5fcrr · Mouse

In slices, light activation of ChR2-expressing ventral CA1 axons evoked a monosynaptic EPSP in BA principal neurons, followed by disynaptic IPSPs that were abolished by glutamate receptor antagonists. In vivo, theta burst photostimulation suppressed principal neuron firing.

Figs. 2D-E, 3A-C, 3H-J, S4

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

CA1 (Field CA1) MBA:382 projects to LA (Lateral amygdalar nucleus) MBA:131 · Mouse

Only sparse ChR2-YFP-positive ventral CA1 fibres were seen in the lateral amygdala.

Fig. 2B

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