Amygdala-hippocampus somatostatin interneuron beta-synchrony underlies a cross-species biomarker of emotional state Amygdala-hippocampus (HPC) beta-coherence variance / bursts This study shows that beta-frequency communication between the amygdala and hippocampus tracks emotional state in both humans and mice. The biomarker, based on beta-frequency coherence between these structures, reflects synchronization between somatostatin (SST+) interneurons in the amygdala and hippocampus. This synchronization dynamically predicts approach-avoidance decisions and can be modulated by optogenetic manipulation of phase. The study demonstrates that this biomarker is a causal driver of behavior, not just a readout. BLA-SST+ neurons directly inhibit ventral hippocampus SST+ interneurons, and their synchronization is crucial for emotional processing. The findings reveal a novel mechanism where interregional synchronization, specific to frequency, phase, and cell type, controls emotional processing. The study also shows that beta-coherence bursts, which occur on subsecond timescales, predict anxiety-related behaviors on fast timescales. These bursts are associated with SST+ interneuron synchronization and are influenced by phase relationships between BLA and hippocampus neurons. The results highlight the role of precise phase relationships between specific cell types in creating network states that control emotional responses. The study also shows that manipulating beta-synchrony in SST+ interneurons bidirectionally modulates anxiety-related behaviors. These findings establish that beta-synchrony between amygdala and hippocampus SST+ interneurons is a cross-species biomarker of emotional state.Amygdala-hippocampus somatostatin interneuron beta-synchrony underlies a cross-species biomarker of emotional state Amygdala-hippocampus (HPC) beta-coherence variance / bursts This study shows that beta-frequency communication between the amygdala and hippocampus tracks emotional state in both humans and mice. The biomarker, based on beta-frequency coherence between these structures, reflects synchronization between somatostatin (SST+) interneurons in the amygdala and hippocampus. This synchronization dynamically predicts approach-avoidance decisions and can be modulated by optogenetic manipulation of phase. The study demonstrates that this biomarker is a causal driver of behavior, not just a readout. BLA-SST+ neurons directly inhibit ventral hippocampus SST+ interneurons, and their synchronization is crucial for emotional processing. The findings reveal a novel mechanism where interregional synchronization, specific to frequency, phase, and cell type, controls emotional processing. The study also shows that beta-coherence bursts, which occur on subsecond timescales, predict anxiety-related behaviors on fast timescales. These bursts are associated with SST+ interneuron synchronization and are influenced by phase relationships between BLA and hippocampus neurons. The results highlight the role of precise phase relationships between specific cell types in creating network states that control emotional responses. The study also shows that manipulating beta-synchrony in SST+ interneurons bidirectionally modulates anxiety-related behaviors. These findings establish that beta-synchrony between amygdala and hippocampus SST+ interneurons is a cross-species biomarker of emotional state.