Compressed spinal cord injury (CSCI) has become a global issue due to vertebra fracture, spinal tuberculosis, ligamenta flava rigidification, tumor in marrow, epidural hematoma etc.It affects a vast patient population and represents a huge unmet therapeutic need.The main pathological changes are apoptosis of neurons and oligodendrocytes (oligos)which result in demyelination.Oligos are involved in axon myelinization, and differentiated from oligodendrocyte precursor cells (OPCs).The growth and development of oligos and OPCs are regulated by the oligodendrocyte precursor cell transcription factors Oligl/2 and Id2 (Inhibitor of DNA binding-2).In our previous studies, the results achieved are as follows:neurons and oligos underwent apoptosis which led to wallerian degeneration in CSCI;transmission electron microscopy revealed distal axons degenerated,of early stage of wallerian degeneration, dozens of single layer-membrane vesicles,sometimes accompanied by a normally-shaped mitochondria within 24hours after CSCI;axon sheaths disintegrated largely in 72hours;axon starts to regenerate in 5days after CSCI, it is disproportional between the diameter of axon and the thickness of myelin;Id2 was co-labelled with oligodendrocytes, and overexpressed in oligos;Western blotting of Id2 revealed increased levels significantly with time going by;electronacupuncture stimulation induced OPCs proliferation and Id2 down-regulation in the compressed spinal cord of rats.Our findings demonstrate that the wallerian degeneration of the compressed spinal cord of rats aggravates with time going by;Id2 proteins regulate oligodendrocytes by enhancing proliferation and inhibiting differentiation after CSCI;electronacupuncture stimulation could be used to promote remyelination and recovery of function in CSCI by inducing OPCs proliferation which differentiates into oligos involved in axon myelinization.