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Updated: May 30, 2025

Intracranial Pharmacotherapy and Pain Assays in Rodents
Published on: April 9, 2019
Involvement of a central amygdaloid nucleus-lateral habenular nucleus pathway in the processing of formalin-induced
Wen-Jun Zhao1, Hui-Jie Feng2, Shan Wang3
1Department of Anatomy, Histology and Embryology, K. K. Leung Brain Research Centre, The Fourth Military Medical University, Xi'an 710032, China; Institute of Orthopedics, Xijing Hospital, the Fourth Military Medical University, Xi'an, China; Innovation Researh Institute, Xijing Hopsital, The Fourth Military Medical University, Xi'an 710032, China.
Abstract:
The central amygdaloid nucleus (CeA) and the lateral habenular nucleus (LHb) are essential nuclei playing modulatory roles in encoding noxious stimuli. Their interaction has recently been demonstrated in chronic pain-induced depression. However, little is known about the CeA-LHb pathway in a formalin-induced pain model. In the present study, we aimed to clarify whether the CeA-LHb pathway modulates the formalin-induced pain model using a neuroanatomical tracing method combined with a designer receptor exclusively activated by a designer drugs strategy (DREADD). The results revealed that the CeA predominantly sends projections to vesicular glutamate transporter-2 (VGluT2)-expressing neurons of the LHb, and inhibition of LHb function exhibits an analgesic effect in the formalin-induced pain model. Furthermore, activating the CeA-LHb pathway significantly attenuates pain sensation only in phase 2 of formalin-induced pain in mice. The present results indicate the participation of the LHb in inflammatory pain sensation and reveal a CeA-LHbVGluT2 pathway that displays analgesic effects in a formalin pain model.
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