BACKGROUND:　Studies　have　demonstrated　that　cauda　equina　compression　results　in　apoptosis　of　motor　neurons　in　the　spinal　cord.　The　combination　of　p75　neurotrophin　receptor　(p75NTR)　and　precursor　of　nerve　growth　factor　(pro-NGF)　expression　initiates　the　apoptotic　pathway　and　induces　neuronal　apoptosis.　However,　few　reports　have　focused　on　the　p75-mediated　mechanism　of　neuronal　apoptosis　following　cauda　equine　compression　injury　OBJECTIVE:　To　determine　apoptosis　of　spinal　cord　neurons　and　activation　of　the　pro-NGF-p75NTR-JNK(c-Jun　N-terminal　kinase)　signal　pathway　in　rats　following　cauda　equina　compression,　and　to　verify　experimental　outcomes.　DESIGN,　TIME　AND　SETTING:　A　randomized,　controlled,　in　vivo　experiment　was　performed　at　the　Medical　Experimental　Center　of　Xi＇an　Jiaotong　University　between　April　and　November　in　2008.　MATERIALS:　Streptavidin-perosidase　kit　was　purchased　from　Wuhan　Boster,　China;　in　situ　end　labeling　detection　kit　was　provided　by　Promega,　USA;　type　AEG-220G　electron　microscope　was　purchased　from　Hitachi,　Japan.　METHODS:　A　total　of　48　healthy,　adult,　female,　Sprague　Dawley　rats　were　randomly　assigned　to　three　groups:　normal　(n　=　6),　sham-surgery　(n　=　6),　and　compression　(n　=　36).　The　compression　group　was　randomly　assigned　to　six　subsets　at　1,　3,　5,　7,　14,　and　28　days,　respectively,　with　6　rats　in　each　subset.　A　cylindrical　silica　gel　stick　was　implanted　into　the　rats　to　compress　75%　of　the　vertebral　canal　in　the　compression　group;　in　the　sham-surgery　group,　only　vertebral　resection　was　performed;　and　no　procedures　were　performed　in　the　normal　group.　MAIN　OUTCOME　MEASURES:　At　1,　3,　5,　7,　14,　and　28　days　following　compression,　L(2-3)　spinal　cord　segments　were　processed　for　immunohistochemistry,　in　situ　cell　apoptosis　detection,　and　transmission　electron　microscopy　observation.　Nissl　staining　was　used　to　observe　neuronal　survival　in　the　L(2)　spinal　cord　segment.　Immunohistochemistry　was　applied　to　detect　expressions　of　pro-NGF,　p75NTR,　and　JNK　in　the　L(2)　segment.　TUNEL　fluorometric　method　was　used　to　observe　apoptosis　of　neurons　in　the　L(2)　segment.　RESULTS:　In　the　normal　and　sham-surgery　groups,　little　neuronal　apoptosis　was　observed　in　the　L2-3　spinal　cord　segment.　At　3　days　after　compression　injury,　pro-NGF,　p75NTR　and　JNK　expression　was　observed　in　the　spinal　cord.　Expression　levels　reached　a　peak　at　7　days,　and　then　gradually　decreased.　In　the　compression　and　sham-surgery　groups,　neurons　primarily　expressed　pro-NGF　and　p75NTR.　The　number　of　JNK-positive　neurons　in　the　compression　group　was　dramatically　increased　compared　with　the　sham-surgery　group　(P　＜　0.05).　A　few　neurons　were　apoptotic　in　the　spinal　cord　1　day　after　compression　injury.　The　number　of　apoptotic　neurons　gradually　increased　and　reached　a　peak　at　7　days,　and　subsequently　decreased.　Apoptosis　was　still　detectable　at　28　days.　There　was　a　positive　correlation　between　p75NTR　expression　and　neuronal　apoptosis　(r　=　0.　75,　P　＜　0.　05).　CONCLUSION:　Following　cauda　equina　compression　injury,　apoptosis　of　spinal　cord　neurons　was　observed.　The　compression-induced　neuronal　apoptosis　was　associated　with　p75NTR　expression　in　the　L(2-3)　spinal　cord　segment.