Abstract
Accumulation of stressful events can render individuals susceptible to develop epilepsy and comorbidities. Whether such vulnerability can be predicted and reversed is not known. Here we show that social defeat, although not producing depression by itself, produced in 50% of rats reduced threshold for status epilepticus (SE), accelerated epileptogenesis, and once epilepsy was induced, depression-like profile and cognitive deficits. Low serum brain-derived neurotrophic factor (BDNF) levels measured before SE identified this vulnerable population. Treatment with a BDNF analog before SE prevented the occurrence of comorbidities. Thus, vulnerability to comorbidities after epilepsy onset due to unresolved past stressful events may be predicted and reversed.
© 2015 American Neurological Association.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Allostasis
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Animals
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Brain-Derived Neurotrophic Factor / drug effects
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Brain-Derived Neurotrophic Factor / metabolism*
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Cognition Disorders / metabolism*
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Cognition Disorders / psychology
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Depression / metabolism*
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Depression / psychology
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Disease Models, Animal
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Epilepsy / chemically induced
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Epilepsy / metabolism
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Epilepsy / psychology
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Excitatory Amino Acid Agonists / toxicity
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Flavones / pharmacology
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Hypothalamo-Hypophyseal System / drug effects
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Hypothalamo-Hypophyseal System / metabolism*
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Kainic Acid / toxicity
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Male
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Pituitary-Adrenal System / drug effects
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Pituitary-Adrenal System / metabolism*
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Rats
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Rats, Sprague-Dawley
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Social Environment*
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Status Epilepticus / chemically induced
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Status Epilepticus / metabolism*
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Stress, Psychological / metabolism*
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Stress, Psychological / psychology
Substances
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6,7-dihydroxyflavone
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Brain-Derived Neurotrophic Factor
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Excitatory Amino Acid Agonists
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Flavones
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Kainic Acid