| Summary: | Summary: Impaired interhemispheric connectivity is commonly found in various psychiatric disorders, although how interhemispheric connectivity regulates brain function remains elusive. Here, we use the mouse amygdala, a brain region that is critical for social interaction and fear memory, as a model to demonstrate that contralateral connectivity intensifies the synaptic response of basolateral amygdalae (BLA) and regulates amygdala-dependent behaviors. Retrograde tracing and c-FOS expression indicate that contralateral afferents widely innervate BLA non-randomly and that some BLA neurons innervate both contralateral BLA and the ipsilateral central amygdala (CeA). Our optogenetic and electrophysiological studies further suggest that contralateral BLA input results in the synaptic facilitation of BLA neurons, thereby intensifying the responses to cortical and thalamic stimulations. Finally, pharmacological inhibition and chemogenetic disconnection demonstrate that BLA contralateral facilitation is required for social interaction and memory. Our study suggests that interhemispheric connectivity potentiates the synaptic dynamics of BLA neurons and is critical for the full activation and functionality of amygdalae. : Huang et al. show that contralateral innervation between two basolateral amygdalae (BLA) in the two brain hemispheres evokes the synaptic activity of BLA and intensifies the BLA response to ipsilateral afferents, including cortical and thalamic inputs. BLA contralateral connectivity is required for amygdala-dependent behaviors, including social interaction and memory. Keywords: amygdala, anterior commissure, associative memory, contralateral innervation, social interaction, synaptic facilitation
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