The Effect of Acupuncture on the Morphology and Neural Coding Damage of the Central Amygdala in Mice with Chronic Inflammatory Pain and Depression.

Abstract

Purpose: Observing the effects and roles of acupuncture on the morphology and neural coding damage of central amygdala (CeA) neurons in chronic inflammatory pain with depression (CIPD) mice and exploring the central nervous mechanism of acupuncture intervention in CIPD.

Methods: A CIPD model was established by injecting Complete Freund's Adjuvant (CFA) into the left hind foot. Using paw withdrawal latency (PWLs), forced swimming, and open field tests, 40 mice with successfully replicated models were selected and randomly divided into a model group, acupuncture group, and sham acupuncture group, with 12 mice in each group. After treatment, Nissl staining was used to observe the morphology of CeA neurons and the number of Nissl bodies. In vivo multi-channel recordings measured the spontaneous firing frequency, waveform amplitude, inter-spike interval (ISI), and power spectral density (PSD) of CeA neurons.

Results: The PWLs in the model and sham acupuncture groups were shortened, the activity time and distance in the central region were reduced, and the forced swimming immobility time increased. The arrangement of CeA neurons is sparse, neurons are damaged, and the number of Nissl bodies is reduced; CeA neurons exhibit abnormal changes in spatiotemporal patterns, with a decrease in spontaneous discharge frequency, discharge amplitude, PSD, and an increase in ISI. The acupuncture group showed prolonged PWLs, increased activity time and distance in the central region, and decreased immobility during forced swimming. The loss of CeA neurons decreased, the cells were arranged neatly, the nucleoli were evident, and the number of Nissl bodies increased. The damage to CeA neural coding was significantly improved, with increased spontaneous discharge frequency, discharge amplitude, PSD, and shortened ISI.

Conclusion: Acupuncture may alleviate pain and depressive-like behaviors in CIPD mice and reduce neuronal damage, possibly through mechanisms related to improving the spatiotemporal characteristics of neural coding impairments in the CeA brain region.