The expression of glutamate transporters (GLAST) protein downregulate in spine in bone cancer mice

Abstract

Objective To investigate the expression of glutamate transporter (GLAST) in spine in bone cancer mice. Methods 35 mice were randomly assigned into bone cancer pain model group (Ca group) (n =30) and sham group(n =5). The bone cancer pain model was made by injecting 2 x 105 NCTC 2472 ceils suspended in 20 μl of a minimal essential medium to the medullary cavity of the fight distal femur. The sham group was only injected 20 p,l medium without NCTC 2472 ceils. Mechanical withdraw threshold (MWT) and paw withdrawal latencies (PWL) to radiant heat stimulation of Ca group were measured pre-injection and on the lst,3rd、7th、10th,14th,21st day after injection. The development of the bone tumor and structural damage in the bone were assessed by X-ray scan pre-injection and on the 7th,14th、21st day. Mice were decapitated after the behavior test in the time point of lst、3rd、7th、10th、14th、21st day and the right lumbar spinal cord enlargement was removed. The right lumbar spinal cord enlargement of the sham group was removed directly. The expression of glutamate transporters in the spine were studied by Western blot. Results The MWT of the right foot of Ca group decreased significantly on day 7 compared with that before inoculation procedure (P < 0.05 ) and continued to decrease until 21st day after innoculation procedures. The PWL of the fight foot of Ca group decreased on days 14 significantly compared with that before inoculation procedure (P <0.05) and continued to decrease until 21st day after innoculation procedures. The X-ray scan of the femur showed small pits of destruction in the distal of the bone on the 7th day and increased pitted appearance on the 14th day. Bone loss increased and displaced skeletal fracture appeared on the 21 st day. The expression of the protein content of GLAST decreased from day 10 and decreased significantly by day 14 and continuously decreased till day 21 ( P <0.01 ). Conclusion Downregulation of spinal glutamate transporter was involved in the forming of bone cancer pain. Key words: bone cancer pain; glutamate transporter; spinal cord; allodynia