Host: Prof. Dongmin Yin, East China Normal University
Abstract
Systemic inflammatory response is a pathological process that may occur after infection, surgery, or trauma. It not only affects the immune system but can also involve the central nervous system, leading to emotional disorders such as anxiety and depression. In the basolateral amygdala (BLA), neurons and microglia are considered to play key roles in the development of inflammation-related anxiety; however, the interaction mechanisms between them during anxiety formation remain unclear.
This study found that inflammatory stimulation can significantly activate microglia in the BLA, thereby enhancing excitatory synaptic transmission and increasing the intrinsic excitability of neurons. Transcriptomic analysis suggested that TNF-α is a key factor mediating this intercellular communication. Mechanistic studies showed that microglia promote neuronal plasticity changes by releasing TNF-α and activating the corresponding receptor signaling on neurons. In addition, single-cell sequencing data indicated that a type of neuronal potassium channel plays an important role in regulating the excitability of BLA neurons. Functional verification further confirmed that modulation of this channel can affect neuronal plasticity changes and anxiety-like behaviors.
In summary, this study systematically reveals that under inflammatory conditions, microglia in the BLA enhance neuronal activity through the TNF-α signaling pathway, and cooperate with ion channel–dependent excitability regulation mechanisms to jointly drive the formation of anxiety-like behaviors. These findings deepen the understanding of neuro-immune interactions within the amygdala and provide a new direction for intervention strategies for inflammation-related emotional disorders.
This event is open to the NYU Shanghai, East China Normal University, and Neuroscience community.