Cervical spondylotic myelopathy (CSM) is a common spinal cord dysfunction disease with complex symptoms in clinical presentation. Resting state fMRI (rsfMRI) has been introduced to study the mechanism of neural development of CSM. However, most of those studies focused on intrinsic functional connectivity rather than intrinsic regional neural activity level which is also frequently analyzed in rsfMRI studies. Thus, this study aims to explore whether the level of neural activity changes on the myelopathic cervical cord and evaluate the possible relationship between this change and clinical symptoms through amplitude of low frequency fluctuation (ALFF). Eighteen CSM patients and twenty five healthy subjects participated in rsfMRI scanning. ALFF was investigated on each patient and subject. The results suggested that ALFF values were higher in the CSM patients at all cervical segments, compared to the healthy controls. The severity of myelopathy was associated with the increase of ALFF. This finding would enrich our understanding on the neural development mechanism of CSM.

Mechanical stress has detrimental effects on cartilaginous endplate chondrocytes due to apoptosis in vivo and in vitro. In this study, we investigated the possible apoptosis signaling pathways induced by mechanical stress in cultured rat cervical endplate chondrocytes. Static mechanical load significantly reduced cell viability in a time- and load-dependent manner, as demonstrated by the Cell Counting Kit-8 (CCK-8) assay. Chondrocyte apoptosis induced by mechanical stress was confirmed by annexin V/propidium iodide (PI) staining and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL). Western blot analysis revealed that static load-induced chondrocyte apoptosis was accompanied by increased phosphorylation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 mitogen-activated protein kinase (MAPK). The loss of mitochondrial membrane potential (ΔΨm), increased Cytochrome c release, and activated Caspase-9 and Caspase-3, indicating that the mitochondrial pathway is involved in mechanical stress-induced chondrocyte apoptosis. Treatment with inhibitors of JNK (SP600125), p38 MAPK (SB203580), and ERK (PD98059) prior to mechanical stimulation reversed both the static load-induced chondrocyte apoptosis and the activation of JNK, p38 MAPK, and ERK. Taken together, the data presented in this study demonstrate that mechanical stress induces apoptosis in rat cervical endplate chondrocytes through the MAPK-mediated mitochondrial apoptotic pathway.