Amygdala microglia modify neuronal plasticity via complement C1q/C3-CR3 signaling and contribute to visceral pain in a rat model
Tian Yuan, Albert Orock, Beverley Greenwood–Van Meerveld
Abstract
Patients with irritable bowel syndrome (IBS) show altered amygdala activity. We showed previously that stress induces visceral hypersensitivity partially through microglia-modulated synaptic plasticity in the central nucleus of the amygdala (CeA). Our current data suggest that the C1q/C3-CR3 cascade initiates microglia-mediated synaptic remodeling in the CeA. Blocking C3-CR3 interaction attenuates stress-induced visceral hypersensitivity. These findings uncover a role of microglia-synapse signaling in the brain-gut regulation and support a future therapeutic target to treat visceral pain.
Topics & Concepts
MicrogliaNeuroscienceIrritable bowel syndromeCentral nucleus of the amygdalaVisceral painAmygdalaSynaptic plasticityMedicineNeuroplasticitySynapseNeuroinflammationInflammationPsychologyReceptorInternal medicineNociceptionNeuroinflammation and Neurodegeneration MechanismsGastrointestinal motility and disordersNeuropeptides and Animal Physiology