4 research outputs found
The Effects Of Minocycline On The Hippocampus In Lithium-Pilocarpine Induced Status Epilepticus In Rat: Relations With Microglial/Astrocytic Activation And Serum Mob Level
AIM: To investigate possible correlations between serum S100B levels and microglial/astrocytic activation in status epilepticus (SE) in lithium-pilocarpine-exposed rat hippocampi and whether serum S100B levels linearly reflect neuroinflammation. Additionally, to assess the effects of minocycline (M), an inhibitor of neuroinflammation. MATERIAL and METHODS: Rats were divided into 4 groups (6/group), namely, control (C), sham, SE, and SE+M. Animals were exposed to lithium-pilocarpine to induce SE in the SE and SE+M groups. Cardiac blood was collected to measure S100B levels, and coronal brain sections including the hippocampus were prepared to examine microglial/astrocytic activation and to evaluate neuroinflammation at day 7 of SE. RESULTS: Serum S100B levels, OX42 (+) microglia in CA1, and GFAP (+) astrocytes in both CA1 and dentate gyrus (DG) were higher in the SE+M group than in the C group. Most importantly, highly positive correlations were found between S100B levels and microglial activation in CA1, apart from astrocytic activation in CA1 and DG. Unexpectedly, microglial activation in CA1 and astrocytic activation in DG were also enhanced in the SE+M group compared with the C group. Moreover, M administration reversed the neuronal loss observed in DG during SE. CONCLUSION: These results suggest that serum S100B is a candidate biomarker for monitoring neuroinflammation and that it may also help predict diagnosis and prognosis.WoSScopu
Investigation of the Possible Protective Effects of Ketamine and Dantrolene on the Hippocampal Apoptosis and Spatial Learning in Rats Exposed to Repeated Electroconvulsive Seizures as a Model of Status Epilepticus
AIM: To evaluate the possible neuroprotective effects of ketamine and
dantrolene on the hippocampal apoptosis and spatial learning in rats
exposed to repeated electroconvulsive seizures (ECS) as a model of
status epilepticus (SE).
MATERIAL and METHODS: Twenty-four rats were assigned to 4 groups. 1st
Group was Sham. 2nd Group was ECS: ECS was induced by ear electrodes via
electrical stimulation. The same ECS protocol was applied to the 3th and
4th Groups which received ketamine (40 mg/kg s.c.) or dantrolene (5
mg/kg i.p.) 1 h before each ECS, respectively. Following 30 days of
recovery, the cognitive status of the animals was evaluated via Morris
Water Maze (MWM). The same experimental protocol was repeated 14 days
afterward to evaluate the retention of the memory. Hippocampal apoptosis
was examined in corresponding experimental groups.
RESULTS: All the animals in four groups learned the task with no
significant difference between groups in MWM. The ECS+ketamine group
showed memory impairment 14 days afterward. ECS+dantrolene group was not
different from controls. ECS caused long term apoptotic processes in
dentate gyrus (DG) and non-apoptotic neuronal injury in CA1 and CA2.
CONCLUSION: Dantrolene and ketamine inhibited apoptosis and showed
neuroprotective effects. Although ketamine and dantrolene inhibited
ECS-induced apoptosis and non-apoptotic injury, they did not produce
similar effects on memory retention. It will be warranted to evaluate
cognitive dysfunction by taking into consideration the other factors in
addition to apoptosis and neurodegenerative changes