Postnatal systemic inflammation exacerbates impairment of hippocampal synaptic plasticity in an animal seizure model

Yuan Hao Chen, Tung Tai Kuo, Ming Ting Chu, Hsin I. Ma, Yung Hsiao Chiang, Eagle Yi Kung Huang

研究成果: 雜誌貢獻文章

12 引文 (Scopus)

摘要

Objective: To investigate the effects of systemic inflammation in the critical postnatal stages on neurophysiological actions of immune processes and neural plasticity in adult rats after kainic acid (KA)-induced seizures. Methods: To determine changes in hippocampal synaptic plasticity after postnatal central nervous system inflammatory responses and seizure attacks, we performed intraperitoneal injections of lipopolysaccharide (LPS) in postnatal Sprague Dawley rats on day 14 (P14) to induce central nervous system inflammation. We then used a KA tail vein injection on P35 to induce seizure attacks. We compared the variability in synaptic plasticity in the hippocampal Schaffer collateral-CA1 region of seizure animals with or without LPS-induced inflammation preconditioning. Results: P14 injection of LPS increased susceptibility to seizures, while treatment with KA on P35 induced seizures. Long-term potentiation (LTP) of the Schaffer collateral-CA1 region was impaired in seizure animals, and this effect was more pronounced in the P14 LPS injection group. Fluoro-Jade staining revealed an increase in degenerated hippocampal CA1 pyramidal cells in the P14 LPS injection group. Cytokine expression in the hippocampus in the pre-, peri-and postictus periods was greater in P14 LPS rats than in saline-treated rats. Conclusions: Intraperitoneal LPS injection on P14 induces higher cytokine secretion after KA-induced seizures, enhancing neuronal excitability, shortening seizure onset time and exacerbating neuronal degeneration and impairment of LTP formation in the hippocampal Schaffer collateral-CA1 region. Central nervous system inflammation during critical stages of childhood development could disrupt the balance needed for neurophysiological actions of immune processes, producing direct, pernicious effects on memory, neural plasticity and neurogenesis into adulthood.

原文英語
頁(從 - 到)223-232
頁數10
期刊NeuroImmunoModulation
20
發行號4
DOIs
出版狀態已發佈 - 六月 2013

指紋

Neuronal Plasticity
Seizures
Animal Models
Lipopolysaccharides
Inflammation
Kainic Acid
Hippocampus
Injections
Central Nervous System
Long-Term Potentiation
Intraperitoneal Injections
Cytokines
Pyramidal Cells
Neurogenesis
Sprague Dawley Rats
Tail
Veins
Staining and Labeling

ASJC Scopus subject areas

  • Endocrinology
  • Immunology
  • Endocrine and Autonomic Systems
  • Neurology

引用此文

Postnatal systemic inflammation exacerbates impairment of hippocampal synaptic plasticity in an animal seizure model. / Chen, Yuan Hao; Kuo, Tung Tai; Chu, Ming Ting; Ma, Hsin I.; Chiang, Yung Hsiao; Huang, Eagle Yi Kung.

於: NeuroImmunoModulation, 卷 20, 編號 4, 06.2013, p. 223-232.

研究成果: 雜誌貢獻文章

Chen, Yuan Hao ; Kuo, Tung Tai ; Chu, Ming Ting ; Ma, Hsin I. ; Chiang, Yung Hsiao ; Huang, Eagle Yi Kung. / Postnatal systemic inflammation exacerbates impairment of hippocampal synaptic plasticity in an animal seizure model. 於: NeuroImmunoModulation. 2013 ; 卷 20, 編號 4. 頁 223-232.
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title = "Postnatal systemic inflammation exacerbates impairment of hippocampal synaptic plasticity in an animal seizure model",
abstract = "Objective: To investigate the effects of systemic inflammation in the critical postnatal stages on neurophysiological actions of immune processes and neural plasticity in adult rats after kainic acid (KA)-induced seizures. Methods: To determine changes in hippocampal synaptic plasticity after postnatal central nervous system inflammatory responses and seizure attacks, we performed intraperitoneal injections of lipopolysaccharide (LPS) in postnatal Sprague Dawley rats on day 14 (P14) to induce central nervous system inflammation. We then used a KA tail vein injection on P35 to induce seizure attacks. We compared the variability in synaptic plasticity in the hippocampal Schaffer collateral-CA1 region of seizure animals with or without LPS-induced inflammation preconditioning. Results: P14 injection of LPS increased susceptibility to seizures, while treatment with KA on P35 induced seizures. Long-term potentiation (LTP) of the Schaffer collateral-CA1 region was impaired in seizure animals, and this effect was more pronounced in the P14 LPS injection group. Fluoro-Jade staining revealed an increase in degenerated hippocampal CA1 pyramidal cells in the P14 LPS injection group. Cytokine expression in the hippocampus in the pre-, peri-and postictus periods was greater in P14 LPS rats than in saline-treated rats. Conclusions: Intraperitoneal LPS injection on P14 induces higher cytokine secretion after KA-induced seizures, enhancing neuronal excitability, shortening seizure onset time and exacerbating neuronal degeneration and impairment of LTP formation in the hippocampal Schaffer collateral-CA1 region. Central nervous system inflammation during critical stages of childhood development could disrupt the balance needed for neurophysiological actions of immune processes, producing direct, pernicious effects on memory, neural plasticity and neurogenesis into adulthood.",
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T1 - Postnatal systemic inflammation exacerbates impairment of hippocampal synaptic plasticity in an animal seizure model

AU - Chen, Yuan Hao

AU - Kuo, Tung Tai

AU - Chu, Ming Ting

AU - Ma, Hsin I.

AU - Chiang, Yung Hsiao

AU - Huang, Eagle Yi Kung

PY - 2013/6

Y1 - 2013/6

N2 - Objective: To investigate the effects of systemic inflammation in the critical postnatal stages on neurophysiological actions of immune processes and neural plasticity in adult rats after kainic acid (KA)-induced seizures. Methods: To determine changes in hippocampal synaptic plasticity after postnatal central nervous system inflammatory responses and seizure attacks, we performed intraperitoneal injections of lipopolysaccharide (LPS) in postnatal Sprague Dawley rats on day 14 (P14) to induce central nervous system inflammation. We then used a KA tail vein injection on P35 to induce seizure attacks. We compared the variability in synaptic plasticity in the hippocampal Schaffer collateral-CA1 region of seizure animals with or without LPS-induced inflammation preconditioning. Results: P14 injection of LPS increased susceptibility to seizures, while treatment with KA on P35 induced seizures. Long-term potentiation (LTP) of the Schaffer collateral-CA1 region was impaired in seizure animals, and this effect was more pronounced in the P14 LPS injection group. Fluoro-Jade staining revealed an increase in degenerated hippocampal CA1 pyramidal cells in the P14 LPS injection group. Cytokine expression in the hippocampus in the pre-, peri-and postictus periods was greater in P14 LPS rats than in saline-treated rats. Conclusions: Intraperitoneal LPS injection on P14 induces higher cytokine secretion after KA-induced seizures, enhancing neuronal excitability, shortening seizure onset time and exacerbating neuronal degeneration and impairment of LTP formation in the hippocampal Schaffer collateral-CA1 region. Central nervous system inflammation during critical stages of childhood development could disrupt the balance needed for neurophysiological actions of immune processes, producing direct, pernicious effects on memory, neural plasticity and neurogenesis into adulthood.

AB - Objective: To investigate the effects of systemic inflammation in the critical postnatal stages on neurophysiological actions of immune processes and neural plasticity in adult rats after kainic acid (KA)-induced seizures. Methods: To determine changes in hippocampal synaptic plasticity after postnatal central nervous system inflammatory responses and seizure attacks, we performed intraperitoneal injections of lipopolysaccharide (LPS) in postnatal Sprague Dawley rats on day 14 (P14) to induce central nervous system inflammation. We then used a KA tail vein injection on P35 to induce seizure attacks. We compared the variability in synaptic plasticity in the hippocampal Schaffer collateral-CA1 region of seizure animals with or without LPS-induced inflammation preconditioning. Results: P14 injection of LPS increased susceptibility to seizures, while treatment with KA on P35 induced seizures. Long-term potentiation (LTP) of the Schaffer collateral-CA1 region was impaired in seizure animals, and this effect was more pronounced in the P14 LPS injection group. Fluoro-Jade staining revealed an increase in degenerated hippocampal CA1 pyramidal cells in the P14 LPS injection group. Cytokine expression in the hippocampus in the pre-, peri-and postictus periods was greater in P14 LPS rats than in saline-treated rats. Conclusions: Intraperitoneal LPS injection on P14 induces higher cytokine secretion after KA-induced seizures, enhancing neuronal excitability, shortening seizure onset time and exacerbating neuronal degeneration and impairment of LTP formation in the hippocampal Schaffer collateral-CA1 region. Central nervous system inflammation during critical stages of childhood development could disrupt the balance needed for neurophysiological actions of immune processes, producing direct, pernicious effects on memory, neural plasticity and neurogenesis into adulthood.

KW - Cytokine

KW - Postnatal inflammation

KW - Seizures

KW - Synaptic plasticity

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DO - 10.1159/000348440

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C2 - 23736043

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EP - 232

JO - NeuroImmunoModulation

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SN - 1021-7401

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