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Differential effects between one week and four weeks exposure to same mass of SO 2 on synaptic plasticity in rat hippocampus
Author(s) -
Yao Gaoyi,
Yun Yang,
Sang Nan
Publication year - 2016
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.22093
Subject(s) - synaptophysin , synaptic plasticity , neurotoxicity , glutamate receptor , hippocampus , protein kinase a , postsynaptic density , postsynaptic potential , inhalation exposure , endocrinology , protein kinase c , medicine , nmda receptor , synapse , inhalation , biology , chemistry , neuroscience , anesthesia , kinase , receptor , microbiology and biotechnology , toxicity , immunohistochemistry
Sulfur dioxide (SO 2 ) is a ubiquitous air pollutant. The previous studies have documented the adverse effects of SO 2 on nervous system health, suggesting that acutely SO 2 inhalation at high concentration may be associated with neurotoxicity and increase risk of hospitalization and mortality of many brain disorders. However, the remarkable features of air pollution exposure are lifelong duration and at low concentration; and it is rarely reported that whether there are different responses on synapse when rats inhaled same mass of SO 2 at low concentration with a longer term. In this study, we evaluated the synaptic plasticity in rat hippocampus after exposure to same mass of SO 2 at various concentrations and durations (3.5 and 7 mg/m 3 , 6 h/day, for 4 weeks; and 14 and 28 mg/m 3 , 6 h/day, for 1 week). The results showed that the mRNA level of synaptic plasticity marker Arc, glutamate receptors (GRIA1, GRIA2, GRIN1, GRIN2A, and GRIN2B) and the protein expression of memory related kinase p‐CaMKпα were consistently inhibited by SO 2 both in 1 week and 4 weeks exposure cases; the protein expression of presynaptic marker synaptophysin, postsynaptic density protein 95 (PSD‐95), protein kinase A (PKA), and protein kinase C (PKC) were increased in 1 week exposure case, and decreased in 4 weeks exposure case. Our results indicated that SO 2 inhalation caused differential synaptic injury in 1 week and 4 weeks exposure cases, and implied the differential effects might result from different PKA‐ and/or PKC‐mediated signal pathway. © 2014 Wiley Periodicals, Inc. Environ Toxicol 31: 820–829, 2016.