Table 1.
Number of animals used for each experimental procedure per group.
Fig 1.
Study design and animal groups.
The animals were randomly assigned to one of the four groups. SE, Status Epilepticus; NORT, Novel Object Recognition Task; MWM, Morris Water Maze; Li, Lithium administration; Pil, Pilocarpine; Cef, Ceftriaxone.
Table 2.
Primers used for the cDNA amplification (qPCR).
Fig 2.
Positive effect of ceftriaxone treatment on seizure severity and convulsive behavior in animal models of temporal lobe epilepsy.
The latency to the start of SE (A), number of stage 3 and 4 seizures (B) and average duration of stage 3 and 4 seizures (C) were shown. All data are shown as mean±SEM. # p<0.05, ## p<0.01 compared to the Pil group.
Fig 3.
GLT-1 Expression in the animal groups studied in the acute (72 hours post SE) and chronic (31 days post SE) phase of epileptogenesis in the hippocampus.
Ceftriaxone treatment could increase the level of GLT-1 expression as compared to the untreated epileptic animals (Pil group) both 72 hours (A) and 31 days (B) after model induction. All data are shown as mean±SEM. ** p<0.01, **** p<0.0001 as compared to the Control and ## p<0.01, #### p<0.0001 as compared to the Pil group.
Fig 4.
The effect of temporal lobe epilepsy and ceftriaxone treatment on the total glutamate concentration in the hippocampus in the acute (A) and chronic phase of epileptogenesis (B).
Ceftriaxone treatment of epileptic animals (Pil+Cef group) could decrease glutamate content 72 hours post SE as compared to the untreated epileptic animals. All data are shown as mean±SEM. * p<0.05, ** p<0.01, *** p<0.001 as compared to the Control and ### p<0.001 as compared to the Pil group.
Fig 5.
Glutamine Synthetase (GS) activity in the hippocampus of animals studied 72 hours and 31 days post SE.
Ceftriaxone treatment increase the enzyme activity in the animals of Pil+Cef group as compared to the Pil group during the acute phase of epileptogenesis. All data are shown as mean±SEM. # p<0.05 as compared to the Pil group.
Fig 6.
Spatial learning in the morris water maze navigation task in animals studied 31 days post SE.
The track plots during the course of learning, reversal learning and visible platform trials illustrate the impaired cognitive functions in the animals of the Pil group, while animals in the Pil+Cef group showed a better performance (A). Data on the time to find the escape platform (escape latency) demonstrated the same results (B). Also, this was obvious in the total distance travelled during the trials (C). All data are shown as mean±SEM. * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001 as compared to the Control and ## p<0.01, ### p<0.001, #### p<0.0001 as compared to the Pil group.
Fig 7.
The mean heatmaps and studied parameters during the first (A) and second (B) probe trials.
Temporal lobe epilepsy induction impaired the memory functions of the animals in both probe trials, while the Ceftriaxone treatment could alleviate the memory loss. All data are shown as mean±SEM. * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001 as compared to the Control and # p<0.05, ## p<0.01, ### p<0.001as compared to the Pil group.
Fig 8.
Positive effect of Ceftriaxone treatment on the object recognition memory of epileptic animals.
The heatmaps illustrate the average location of the animals during the testing trial (A). The exploration time of novel and familiar objects were not different among the groups (B), while Ceftriaxone treatment of epileptic animals increased the discrimination index as compared to their epileptic untreated counterparts (C). All data are shown as mean±SEM. **** p<0.0001 as compared to the Control and #### p<0.0001 as compared to the Pil group.