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Fig. 5. NMDA-induced spasms in betamethasone and calpain inhibitor-treated infant rats. The latency (sec) to the onset of flexion spasms induced by intraperitoneal NMDA was measured in control, beta-methasone, and betamethasone+MDL treated P15 rats. The latency to the onset of spasms was increased in the offspring prenatally exposed to betamethasone+MDL compared to that of control and betamethasone group offspring. However, the frequency of spasms was decreased in the offspring prenatally exposed to control and betamethasone+MDL compared to offspring exposed to betamethasone. Statistical significance was assessed by one-way ANOVA. Error bars denote SEM (**p<0.01, ***p<0.001). Representative current traces showing the depolarization of membrane potential by the application of GABA (100 μM) in control, betamethasone treated, and betamethasone+MDL treated groups, arranged from top to bottom (D). Summarized bar graph showing mean of depolarization of membrane potential (E). Summarized data are shown as mean±SEM (**p<0.01, ***p<0.001 compared to respective controls, n=4~8 in each).
Exp Neurobiol. 2019;28:529~536 https://doi.org/10.5607/en.2019.28.4.529
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