Article ; Online: Carvacrol after status epilepticus (SE) prevents recurrent SE, early seizures, cell death, and cognitive decline.
2017 Volume 58, Issue 2, Page(s) 263–273
Abstract: ... to prevent early recurrence of SE, SE-related neuronal damage, and cognitive decline. ... recurrent SE and early seizures in vivo, but had no detectable effect in the hippocampus on paired-pulse ... with carvacrol or saline. We also evaluated TRPM7 receptor expression and quantified seizure-induced cell death ...
| Abstract | Objective: Carvacrol is a naturally occurring monoterpenic phenol that has been suggested to have an action at transient receptor potential cation subfamily M7 (TRPM7) channels, γ-aminobutyric acid (GABA Methods: We performed long-term, continuous wireless electroencephalography (EEG) monitoring in vivo in rats who underwent perforant path stimulation (PPS) to induce SE and were then randomized to treatment with carvacrol or saline. We also evaluated TRPM7 receptor expression and quantified seizure-induced cell death. The alternating T-maze paradigm was used to assess memory function. Results: Immunostaining showed that TRPM7 channels are widely expressed in neurons within the hippocampus. We found that carvacrol inhibited recurrent SE and early seizures in vivo, but had no detectable effect in the hippocampus on paired-pulse inhibition or the fiber volley, indicating that it was not acting through sodium channel inhibition or GABA receptors. Although the development and severity of chronic epilepsy were not altered by carvacrol, cognitive decline was significantly improved in animals treated with carvacrol. In keeping with preserved memory functions in animals treated with carvacrol, carvacrol had a protective effect against SE-induced cell death in CA1 and hilus, the hippocampal regions most affected by cell loss in the PPS epilepsy model. Significance: Carvacrol, a naturally occurring inhibitor of TRPM7 channels, is a novel, promising treatment to prevent early recurrence of SE, SE-related neuronal damage, and cognitive decline. |
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| MeSH term(s) | Animals ; Cell Death/drug effects ; Cognitive Dysfunction/drug therapy ; Cognitive Dysfunction/etiology ; Disease Models, Animal ; Electric Stimulation/adverse effects ; Electrodes, Implanted ; Hippocampus/drug effects ; Hippocampus/metabolism ; In Vitro Techniques ; Male ; Maze Learning/drug effects ; Monoterpenes/therapeutic use ; Neuroprotective Agents/therapeutic use ; Phosphopyruvate Hydratase/metabolism ; Rats ; Rats, Sprague-Dawley ; Recurrence ; Status Epilepticus/complications ; Status Epilepticus/etiology ; Status Epilepticus/prevention & control ; TRPM Cation Channels/metabolism ; Wireless Technology ; gamma-Aminobutyric Acid/metabolism | ||||||||||
| Chemical Substances | Monoterpenes ; Neuroprotective Agents ; TRPM Cation Channels ; gamma-Aminobutyric Acid (56-12-2) ; carvacrol (9B1J4V995Q) ; Trpm7 protein, rat (EC 2.7.11.1) ; Phosphopyruvate Hydratase (EC 4.2.1.11) | ||||||||||
| Language | English | ||||||||||
| Publishing date | 2017-02 | ||||||||||
| Publishing country | United States | ||||||||||
| Document type | Journal Article | ||||||||||
| ZDB-ID | 216382-2 | ||||||||||
| ISSN | 1528-1167 ; 0013-9580 | ||||||||||
| ISSN (online) | 1528-1167 | ||||||||||
| ISSN | 0013-9580 | ||||||||||
| DOI | 10.1111/epi.13645 | ||||||||||
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| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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