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Published on: February 27, 2018
Effect of Androsterone after Pilocarpine-induced Status Epilepticus in Mice
Inja Cho1, Yang-Je Cho2, Hyun-Woo Kim2
1Department of Neurology and Epilepsy Research Institute, Yonsei University College of Medicine, Seoul, Korea ; Brain Korea 21 Plus Project for Medical Science, Yonsei University, Seoul, Korea.
Background And Purpose:
Neurosteroids exert their antiepileptic effects via GABAA and NMDA receptors. Another cell death mechanism is excessive Ca(2+) influx into cells. Calbindin-D28k (CB) is a protein that modulates intracellular Ca(2+) in the nervous system. We evaluated whether androsterone up-regulates the expression of CB and has a neuroprotective effect by controlling Ca(2+) after pilocarpine-induced status epilepticus (SE) in mice.
Methods:
SE was induced in ICR mice by injection of pilocarpine. Two hours after SE, mice were treated intraperitoneally (i.p.) with androsterone (100-200 mg/kg) or vehicle, and compared with other control groups. Two days after injection, immunohistochemical staining for CB was performed using a hippocampal slice from each mice group. We also used cresyl violet staining to compare changes in hippocampal structures.
Results:
Two days after pilocarpine-induced SE, androsterone increased the expression of CB in the hippocampus compared with control SE mice. The number of CB-positive cells was 1±0.4 cells/mm(3) in pilocarpine-only group, 14±1.1 cells/mm(3) in pilocarpine plus androsterone 100 mg group and 29±2.5 cells/mm(3) in pilocarpine plus androsterone 200 mg group (p<0.001).
Conclusions:
These results suggest that the neuroprotective effect of androsterone after pilocarpine- induced SE may be mediated by an increased expression of CB.
Insights
Androsterone boosts Calbindin-D28k (CB) expression in the brain after seizures. This suggests androsterone offers neuroprotection by managing calcium levels, potentially aiding epilepsy treatment.
Area of Science:
- Neuroscience
- Neuropharmacology
- Cellular Biology
Background:
- Neurosteroids are known for their antiepileptic properties, acting on GABAA and NMDA receptors.
- Excessive calcium (Ca2+) influx is a key mechanism in cell death.
- Calbindin-D28k (CB) is a crucial calcium-modulating protein in the nervous system.
Purpose of the Study:
- To investigate if androsterone up-regulates Calbindin-D28k (CB) expression.
- To determine if androsterone provides neuroprotection by controlling intracellular Ca2+.
- To evaluate androsterone's effects following pilocarpine-induced status epilepticus (SE) in a mouse model.
Main Methods:
- Status epilepticus (SE) was induced in mice using pilocarpine.
- Mice received intraperitoneal injections of androsterone (100-200 mg/kg) or vehicle post-SE.
- Immunohistochemical staining for CB and cresyl violet staining were used to assess CB expression and hippocampal structure changes.
Main Results:
- Androsterone significantly increased CB expression in the hippocampus of mice subjected to SE.
- CB-positive cell counts rose from 1±0.4 cells/mm³ in the pilocarpine-only group to 14±1.1 and 29±2.5 cells/mm³ with androsterone treatment (100 and 200 mg/kg, respectively).
- A dose-dependent increase in CB expression was observed with androsterone administration.
Conclusions:
- Androsterone demonstrates a neuroprotective effect in the context of pilocarpine-induced SE.
- The neuroprotective mechanism of androsterone appears to involve the upregulation of Calbindin-D28k (CB) expression.
- This suggests a potential therapeutic role for androsterone in managing seizures and associated neuronal damage.
