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Electroconvulsive Seizures in Rats and Fractionation of Their Hippocampi to Examine Seizure-induced Changes in Postsynaptic Density Proteins
Published on: August 15, 2017
Proteomic Analysis After Status Epilepticus Identifies UCHL1 as Protective Against Hippocampal Injury
James P Reynolds1, Eva M Jimenez-Mateos1, Li Cao2
1Department of Physiology and Medical Physics, Royal College of Surgeons in Ireland, 123 St. Stephen's Green, Dublin 2, Ireland.
Neurochemical Research
|April 12, 2017
Summary
Brief seizures can protect the brain. Loss of the UCHL1 protein after prolonged seizures (status epilepticus) harms neurons, but UCHL1 levels can be increased by rapamycin therapy.
Area of Science:
- Neuroscience
- Biochemistry
Background:
- Brief, non-harmful seizures can induce temporary brain protection against subsequent injurious seizures.
- Status epilepticus (SE) is a prolonged seizure condition that can cause brain injury.
Purpose of the Study:
- To identify protein changes associated with seizure tolerance and injury.
- To investigate the role of ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1) in seizure-induced brain injury and tolerance.
Main Methods:
- Proteomic screening in preconditioned (tolerant) and sham-preconditioned (injured) mice following SE.
- Inhibition of UCHL1 and assessment of its effects on neuronal survival and seizure activity.
- Analysis of UCHL1 and antisense Uchl1 (AsUchl1) expression post-SE.
Main Results:
- Proteins involved in protein trafficking and cytoskeletal regulation were altered following SE.
- Downregulation of UCHL1 was observed in injured mice but not in tolerant mice.
- UCHL1 inhibition exacerbated seizure-induced cell death and disrupted UPS function.
- Post-transcriptional loss of UCHL1 following SE was linked to neuronal damage and hyperexcitability.
Conclusions:
- The post-transcriptional loss of UCHL1 contributes to neuronal injury and hyperexcitability after SE.
- Increasing UCHL1 expression, potentially via AsUchl1 or rapamycin, may offer a novel therapeutic strategy for SE-induced brain damage.
