Objective To investigate the effects of ceftriaxone on depressive-like behavior and changes of hippocampal glutamate transporter-1 (GLT-1) in C57 mice depression model,and to further explore the molecular mechanism of ceftriaxone on antidepressant action.Methods Thirty male C57 mice were randomly divided into control group(group A,n=10),CUS group(group B,n=10) and CUS+ceftriaxone group(group C,n=10).The mice of the CUS group and the CUS+ceftriaxone group were subjected to chronic unpredictable stress (CUS) for 2 sessions per day for 21 days.Then,the mice of the CUS+ceftriaxone group were given ceftriaxone for 21 days.Behavioral changes were assessed by the sucrose preference test and open field test.The GLT-1 protein levels in the hippocampus were detected by Western blot analysis at the end of the ceftriaxone treatment.Results (1) Compared with the control group,the percentage of sucrose preference,the total traveled distance,the moved velocity,and the frequencies of rearing of the CUS group were significantly decreased(P＜0.05) at the 21 days.However,the percentage of sucrose preference ((78.74 ± 3.54) ％),the total traveled distance ((6818.35 ± 505.14) cm),the moved velocity((12.36±0.89) cm/s),and the frequencies of rearing(58.20±4.05) of the CUS+ceftriaxone group at the end of the ceftriaxone treatment were improved significantly compared with the CUS group ((59.46 ± 2.75) ％,(2931.71±271.89) cm,(5.84±0.42) cm/s,(26.20±2.62),P＜0.05).(2) Western blot analysis indicated significant reductions of the GLT-1 protein levels in the hippocampus of CUS group (versus the control mice:P ＜0.05),and chronic ceftriaxone treatment reversed the CUS-induced decrease in the GLT-1 levels(P＜0.05).Conclusion Ceftriaxone might significantly improve depressive-like behavior in C57 mice depression model.Chronic unpredictable stress (CUS) could down-regulate the GLT-1 protein levels in the hippocampus,which are reversed by ceftriaxone.These results further support the notion enhanced expression of the GLT-1 protcin can be molecular mechanism of ceftriaxone on antidepressant action.

Objective To observe the expression of the IGF-1 on the auditory cortex as well as the hippo-campus of rats which underwent longterm exposure to white noise to explore its effects for the repairment of the noise induced damage in the central nervous system.Methods 16 healthy Wistar rats were randomly grouped as chronic noise exposure group(group A)which underwent the longterm noise exposure(100 dB SPL white noise,4 hours per day for 28 days)and control group(group B).The expression of IGF-1 both on the auditory cortex and hippocampus was measured and the ABR waveforms were recorded.ResuIts Compared with the group A,the num-ber of IGF-1 positive neurons as well as the expression of IGF-1 both in the auditory cortex and the hippocampus of the group B increased(P<0.05),the ABR threshold was significantly higher(P<0.05 )after long-term noise exposure.ConcIusion Chronic noise exposure induced the changes of the IGF-1 system which may play a part in the protection for the noise-induced damage of the central nervous system.

OBJECTIVE: To observe the expression of corticotropin-releasing factor-1 receptor in hippocampus of rats model of salicylate induced tinnitus. METHOD: Twenty-four rats were randomly divided into three groups, eight for each group. For Group A and Group B, 10% salicylic sodium solution was intraperitoneal injected each day at the dose of 350 mg/kg for 21 days in Group A and 14 days in Group B. Group C received intraperitoneal injection with the same amount of saline solution each day for 14 days. ABR were tested 2 days before, and 2 hours after the first administration and after the last injection. Immunohistochemical test and Western Blot were utilized to detect the expression of CRF1R in hippocampus for each group. RESULT: ABR thresholds tested 2 days before the first administration of the 3 groups showed no statistically significant difference (P > 0.05). At the time point of 2 hours after the first injection, the ABR thresholds of Group A and Group B rose by 25.90 dB SPL and 25.03 dB SPL compared with that before the administration, respectively (P < 0. 01). After the last administration, the ABR thresholds of Group A and Group B rose 34.91 dB SPL and 32.62 dB SPI. compared with that before the administration, respectively (P < 0.01). The ABR thresholds of Group C showed no significant statistical difference at all the tested time points (P > 0.05). Immunohistochemical test and Western Blot revealed that the expression level of CRF1R in the hippocampus was A > B > C (P < 0.05). CONCLUSION The expression of CRF1R in the hippocampus of salicylate induced tinnitus rat increased with the injection time, illustrating that CRF1R may participate in the mechanism of tinnitus involving the limbic system.
Animals ; Auditory Threshold ; Disease Models, Animal ; Hippocampus ; metabolism ; Injections, Intraperitoneal ; Rats ; Receptors, Corticotropin-Releasing Hormone ; metabolism ; Salicylates ; adverse effects ; Tinnitus ; chemically induced ; metabolism