Hyperthermia aggravates status epilepticus-induced epileptogenesis and neuronal loss in immature rats
Language English Country United States Media print-electronic
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
NS074926
NINDS NIH HHS - United States
NS059704
NINDS NIH HHS - United States
R01 NS013515
NINDS NIH HHS - United States
NS13515
NINDS NIH HHS - United States
I01 BX000273
BLRD VA - United States
U01 NS074926
NINDS NIH HHS - United States
R21 NS059704
NINDS NIH HHS - United States
PubMed
26259902
DOI
10.1016/j.neuroscience.2015.08.006
PII: S0306-4522(15)00729-0
Knihovny.cz E-resources
- Keywords
- EEG monitoring, immature brain, lithium/pilocarpine model, neuronal injury, temperature,
- MeSH
- Adjuvants, Immunologic toxicity MeSH
- Muscarinic Agonists toxicity MeSH
- Anticonvulsants therapeutic use MeSH
- Apoptosis drug effects physiology MeSH
- Cell Death drug effects MeSH
- Time Factors MeSH
- Lithium Chloride toxicity MeSH
- Nerve Degeneration etiology MeSH
- Diazepam therapeutic use MeSH
- Hyperthermia, Induced adverse effects MeSH
- Rats MeSH
- Disease Models, Animal MeSH
- Brain drug effects pathology physiopathology ultrastructure MeSH
- Neurons pathology ultrastructure MeSH
- Neuropil pathology ultrastructure MeSH
- Animals, Newborn MeSH
- Pilocarpine toxicity MeSH
- Rats, Wistar MeSH
- Status Epilepticus etiology MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Research Support, N.I.H., Extramural MeSH
- Names of Substances
- Adjuvants, Immunologic MeSH
- Muscarinic Agonists MeSH
- Anticonvulsants MeSH
- Lithium Chloride MeSH
- Diazepam MeSH
- Pilocarpine MeSH
This study tightly controlled seizure duration and severity during status epilepticus (SE) in postnatal day 10 (P10) rats, in order to isolate hyperthermia as the main variable and to study its consequences. Body temperature was maintained at 39 ± 1 °C in hyperthermic SE rats (HT+SE) or at 35 ± 1 °C in normothermic SE animals (NT+SE) during 30 min of SE, which was induced by lithium-pilocarpine (3 mEq/kg, 60 mg/kg) and terminated by diazepam and cooling to NT. All video/EEG measures of SE severity were similar between HT+SE and NT+SE pups. At 24h, neuronal injury was present in the amygdala in the HT+SE group only, and was far more severe in the hippocampus in HT+SE than NT+SE pups. Separate groups of animals were monitored four months later for spontaneous recurrent seizures (SRS). Only HT+SE animals developed convulsive SRS. Both HT+SE and NT+SE animals developed electrographic SRS (83% vs. 55%), but SRS frequency and severity were higher in hyperthermic animals (12.5 ± 3.5 vs. 4.2 ± 2.0 SRS/day). The density of hilar neurons was lower, thickness of the amygdala and perirhinal cortex was reduced, and lateral ventricles were enlarged in HT+SE over NT+SE littermates and HT/NT controls. In this model, hyperthermia greatly increased the epileptogenicity of SE and its neuropathological sequelae.
References provided by Crossref.org
Epilepsy Research in the Institute of Physiology of the Czech Academy of Sciences in Prague
The outcome of early life status epilepticus-lessons from laboratory animals