ABSTRACT
Glutamate serves as a major excitatory neurotransmitter in the mammalian central nervous system and is stored in synaptic deft by an uptake system that is dependent on the high-affinity glutamate transporters (ETTAs),which locate in the plasma membrane of glial cells and neurons.ETTAs can rapidly terminate the action of glutamate and maintain its normal physiological functions.If the content or function of glutamate transporters is abnormal,it can result in many physiological dysfunctions.Studies have demonstrated that high-affinity glutamate transporters play an important role in the development of chronic pain,which might be a new therapeutic target for the pain.
ABSTRACT
Objective To evaluate the role of spinal c?Jun N?terminal kinase ( JNK ) signaling pathway in incisional pain in rats. Methods Sixty?three adult male Sprague?Dawley rats, weighing 200-250 g, were randomly divided into 3 groups ( n=21 each) using a random number table: incisional pain group ( IP group) , dimethyl sulfoxide ( DMSO) group, and JNK inhibitor SP600125 group ( SP group) . A 1?cm longitudinal incision was made through skin, fascia and muscle of the plantar aspect of the hindpaw in anesthetized rats. In group DMSO, 10% DMSO 10 μl was injected intrathecally at 30 min before surgery. In group SP, SP600125 25 μg (in 10 μl of 10% DMSO) was injected intrathecally at 30 min before sur?gery. Six rats in each group were sacrificed, and the mechanical paw withdrawal threshold ( MWT) and thermal paw withdrawal latency ( TWL) were measured at 24 h before establishment of the model and 2, 6, 24, 48 and 72 h after establishment of the model. After measurement of the pain threshold at 24 h before establishment of the model and 6, 24, 48 and 72 h after establishment of the model, the lumbar segment of the spinal cord was removed for determination of the expression of phosphorylated JNK ( p?JNK) by im?munofluorescence. Results The MWT was significantly lower, the TWL was shorter, and the expression of p?JNK was lower at each time point after establishment of the model than at 24 h before establishment of the model in group IP (P0?05) . Conclusion Spinal JNK signaling pathway is involved in the develop?ment and maintenance of incisional pain in rats.
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Objective To observe effect of muscle basal lamina containing neural stem cells (NSCs) in repair of spinal cord injury.Methods Thirty-six SD rats from the same nest were used in the study and spinal cord hemisection models were induced.The animals were classified to blank control group (clearance of the lesion edge only with isotonic saline),NSCs group (transplantation of NSCs to the edge),NSCs + muscle basal lamina group (transplantation of complex of NSCs and muscle basal lamina to the edge) according to random number table,with 12 rats per group.At weeks 4 and 8,survival and migration of the transplanted cells and compatibility of muscle basal lamina with the host were detected.At weeks 2,4,and 8,the hindlimb function was assayed using BBB scoring system.Results NSCs in NSCs + muscle basal lamina group grew at the lesion edge,migrated to both sides of the edge,and integrated with peripheral tissues.Whereas,few NSCs survived at the lesion edge in NSCs group and inflammatory cell infiltration was notable.At week 2,there was no statistical difference of BBB score among the three groups.At weeks 4 and 8,BBB score in NSCs + muscle basal lamina group (7.92 ± 1.00,11.38 ± 1.51) was significantly higher than that in blank control group (3.82 ± 0.75,3.71 ± 0.76) and NSCs group (6.25 ±1.06,8.25 ± 1.83) (P＜0.05).Conclusion Muscle basal lamina orients growth of NSCs along its lumen,facilitates migration of host cells to ground substance within its lumen,and reduces local inflammatory reaction.
ABSTRACT
@#Objective To investigate the expression of aquaporin (AQP) 1, AQP4, inward rectifying potassium channel 4.1 (Kir4.1) and cytoskeleton features of rat spinal cord astrocytes after cytochalasin D (CytD) intervention. Methods Spinal cord astrocytes isolated from 2~3-day-old rats were cultured till confluency. MTT was used to assess survival rate of astrocytes 2 h, 12 h and 24 h after co-cultured with 0.05 μg/ml, 0.10 μg/ml, 0.20 μg/ml, 0.40 μg/ml, 0.80 μg/ml and 1.00 μg/ml of CytD, respectively. Confocal microscopy was used to observe cytoskeleton features of astrocytes 2 h after co-cultured with 0.05 μg/ml, 0.10 μg/ml, 0.20 μg/ml, 0.40 μg/ml of CytD. The expression of AQP1, AQP4, Kir4.1 mRNA were determined with real-time PCR 2 h after co-cultured with 0.05 μg/ml, 0.10 μg/ml, 0.20 μg/ml, 0.40 μg/ml, 0.80 μg/ml and 1.00 μg/ml of CytD. Results The survival rate of rat spinal cord astrocytes reduced with the time of co-culture and concentration of CytD (P<0.05). The cytoskeleton of astrocytes was reconstructed. The expression of AQP1, AQP4 and Kir4.1 mRNA increased after co- cultured with 0.05~0.40 μg/ml of CytD. Conclusion The appropriate dosage of CytD may remodel the cytoskeleton and increase the mRNA expression of AQP1, AQP4 and Kir4.1 in spinal cord astrocytes of rats.