Potentiation of Divergent Medial Amygdala Pathways Drives Experience-Dependent Aggression Escalation
Aggression
Male
Mice, Inbred C57BL
03 medical and health sciences
Neuronal Plasticity
0302 clinical medicine
Corticomedial Nuclear Complex
Neural Pathways
Animals
Psychological Distress
Synaptic Transmission
3. Good health
DOI:
10.1523/jneurosci.0370-20.2020
Publication Date:
2020-05-18T21:46:50Z
AUTHORS (7)
ABSTRACT
Heightened aggression can be serious concerns for the individual and society at large are symptoms of many psychiatric illnesses, such as post-traumatic stress disorder. The circuit synaptic mechanisms underlying experience-induced increase, however, poorly understood. Here we find that prior attack experience leading to an increase in aggressive behavior, known priming, activates neurons within posterior ventral segment medial amygdala (MeApv). Optogenetic stimulation MeApv using a depression protocol suppresses whereas high-frequency enhances aggression, mimicking experience. Interrogation neural circuitry revealed mediates priming via connections with ventromedial hypothalamus (VmH) bed nucleus stria terminalis (BNST). These pathways undergo NMDAR-dependent potentiation after attack. Furthermore, MeApv–VmH synapses selectively control duration, MeApv–BNST modulate frequency, both no effect on social behavior. Synaptic contributes increased induced by traumatic stress, weakening transmission these blocks aggression. results reveal basis modulation potentially leveraged toward clinical interventions. <b>SIGNIFICANCE STATEMENT</b> have devastating consequences may associated disorders, escalation, identify two between its downstream partners, enhance Notably, circuits naturally occurring stress-induced increase. illustrate experience, which targeted
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