Neonatal proinflammatory stress induces accumulation of corticosterone and interleukin-6 in the hippocampus of juvenile rats: Potential mechanism of synaptic plasticity impairments
| Autor: | D. I. Peregud, A. O. Tishkina, M. Yu. Stepanichev, Mikhail V. Onufriev, Natalia V. Gulyaeva, S. V. Freiman, I. V. Kudryashova |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine medicine.medical_specialty Long-Term Potentiation Hippocampus Hippocampal formation Biology Biochemistry Proinflammatory cytokine 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Stress Physiological Corticosterone Internal medicine medicine Animals Rats Wistar Neuroinflammation Inflammation Neuronal Plasticity Neocortex Interleukin-6 Long-term potentiation General Medicine Rats 030104 developmental biology Endocrinology medicine.anatomical_structure nervous system chemistry Synaptic plasticity 030217 neurology & neurosurgery |
| Zdroj: | Biochemistry (Moscow). 82:275-281 |
| ISSN: | 1608-3040 0006-2979 |
| Popis: | Infectious diseases in early postnatal ontogenesis can induce neuroinflammation, disrupt normal central nervous system development, and contribute to pathogenesis of cerebral pathologies in adults. To study long-term consequences of such early stress, we induced neonatal proinflammatory stress (NPS) by injecting bacterial lipopolysaccharide into rat pups on postnatal days 3 and 5 and then assessed the levels of corticosterone, proinflammatory cytokines and their mRNAs, and neurotrophins and their mRNAs in the hippocampus and neocortex of the one-month-old animals. Long-term potentiation (LTP) was studied in hippocampal slices as an index of synaptic plasticity. NPS-induced impairments of LTP were accompanied by the accumulation of corticosterone and IL-6 in the hippocampus. In the neocortex, a decrease in exon IV BDNF mRNA was detected. We suggest that excessive corticosterone delivery to hippocampal receptors and proinflammatory changes persisting during brain maturation are among the principal molecular mechanisms responsible for NPS-induced neuroplasticity impairments. |
| Databáze: | OpenAIRE |
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